Articlesuuid:c9328811-bcb8-4025-830c-4d12ae9d7b9b;id=42020-06-07T09:32:53Z9874Neck Infections: What the Radiologist Needs to Know2020-04-14T10:06:14-04:002020-04-14T10:06:14-04:00Roberto Kutcher-Diaz, M.D., David Radcliffe, M.D., Hao Lo, M.D., Hemang Kotecha, D.O., Gabriela Santos-Nunez, M.D.<p>Neck infections represent common clinical emergencies. While diagnosis and treatments are often merely clinical, approximately 10% to 20% of deep neck infection complications are potentially life threatening.<sup>1</sup> Common etiologies for head and neck infection include pharyngitis, mastoiditis, and odontogenic infections. Localization and patterns of spread, especially involving the deep cervical spaces, can be challenging for the treating clinician. Clinical manifestations vary based on the age of presentation and infection site. CT of the neck is the first line of imaging in the acute setting.<sup>2</sup> Although anatomy of the head and neck is challenging, knowledge of common imaging patterns and complications is critical for prompt and accurate diagnosis, which will minimize adverse outcomes.<sup>1</sup></p>
<h2>Cervical Fascia</h2>
<p>While there is considerable variation in the description of the cervical fascial layers, a commonly utilized classification system is based on topographic morphology and distinguishes between the superficial and deep fascia, with the deep fascia being further classified into the superficial, middle, and deep layers. The superficial fascia is of limited clinical importance to radiologists as it is a connective layer interposed between the skin and deep fascia. By comparison, the deep fascia is significant to radiologists as understanding fascial boundaries allows for easier detection of disease, more refined differential diagnoses, anticipated routes of disease spread and subsequent complications.<sup>3,4</sup></p>
<p>The first layer of the deep cervical fascia, the superficial layer, is also known as the investing layer. The superficial layer of the deep cervical fascia (SLDCF) encircles the neck with attachment to the spinous processes and ligamentum nuchae posteriorly; hyoid bone anteriorly; the mandible, temporal, and occipital bones superiorly; and the manubrium, clavicles, and scapulae inferiorly. Through its course, the external layer encompasses the stylohyoid and digastric muscles at the level of the suprahyoid neck; the parotid glands superiorly; the sternocleidomastoid muscles anteriorly; and the trapezius muscles posteriorly. The SLDCF is also continuous with the pectoralis major fascia as well as the trapezius and latissimus dorsi fascia.<sup>3,4</sup></p>
<p>The middle layer, also known as the pretracheal layer, can be further broken down into the muscular and visceral divisions. The muscular division encircles the infrahyoid, geniohyoid, and mylohyoid muscles with superior attachment to the hyoid and thyroid cartilage and inferior continuity with the clavipectoral fascia. The visceral division of the pretracheal layer encircles the thyroid, parathyroid glands, trachea, and esophagus. The posterior aspect of the visceral division, also named the buccopharyngeal fascia, extends from the skull base to the thoracic cavity where it attaches to the pericardium. This layer is of particular clinical significance given that the retropharyngeal spaces lies directly posterior to the buccopharyngeal fascia.<sup>3,4</sup></p>
<p>The deep layer of the deep cervical fascia (DLDCF), also known as the prevertebral fascia, attaches to the ligamentum nuchae posteriorly, encircles the paraspinal musculature, attaches to the transverse processes, encircles the prevertebral musculature, and extends anteriorly where it lies immediately posterior to the buccopharyngeal fascia. Superiorly, the DLDCF attaches to the skull base. Inferiorly, DLDCF is contiguous with the anterior longitudinal ligament, contributes to the transversalis fascia, axillary sheath, and Sibson&rsquo;s fascia. Of note, the carotid sheath is considered by some to be included as a portion of the deep fascia, while other sources consider it a separate entity composed of portions of the external, middle, and deep fascial layers.<sup>3,4</sup></p>
<h2>Parapharyngeal Space</h2>
<p>The parapharyngeal space (PPS) is a paired region extending from the skull base to the hyoid bone. From its anterior edge at the pterygomandibular raphe, the lateral border demarcated by SLDCF extends dorsally medial to the masticator space and deep portion of the parotid gland. The posterior margins are defined by the deep layer of the deep cervical fascia DLDCF at the dorsal aspect of the carotid sheath. Several fascial layers within the space define up to three compartments with varying degrees of communication. These compartments are grouped by some authors as prestyloid and poststyloid parapharyngeal spaces, which others term the <em>parapharyngeal space</em> and <em>carotid space</em>, respectively. The former contains fat and minor salivary glands, while the latter contains the internal carotid artery (ICA), internal jugular vein, and cranial nerves IX-XII. In the suprahyoid neck, as opposed to infrahyoid, most authors consider the carotid sheath to be an incomplete structure. At the level of the angle of the mandible and ICA, the carotid space is invested by the same fascial layers as the parapharyngeal space, thus becoming a posterior (retrostyloid) compartment of the latter (<strong>Figure 1</strong>).<sup>5</sup></p>
<h3>Parapharyngeal Infections</h3>
<p>PPS is largely constituted by fat; therefore, pathology arising from the space is relatively uncommon. Its importance relies on multiple anatomic relationships. The PPS serves to corroborate where pathology originates. Adjacent lesions will shift the PPS in different directions.<sup>6</sup> PPS infections typically occur via the palatine tonsil or by spreading from odontogenic, paranasal sinuses, and parotid gland infections.<sup>2</sup> The lymphatic drainage of these structures leads to lymph nodes in the retropharyngeal and PPS.<sup>7</sup></p>
<h2>Pharyngeal Mucosal Space and Peritonsillar Space</h2>
<p>Pharyngeal mucosal space contains both mucosal and lymphoid tissue. The peritonsillar space is a continuation of the pharyngeal mucosal space, which is divided into nasopharyngeal, oropharyngeal, and hypopharyngeal segments. It is bordered by the deep cervical fascia middle layer along the lateral and posterior margins. It is not, however, a true enclosed fascial space because no fascia is present along the airway surface. The retropharyngeal space is located directly posterior, while the parapharyngeal space lies laterally. The intrinsic contents include pharyngeal mucosa, lymphatic ring (adenoids, palatine tonsils, lingual tonsils), minor salivary glands, torus tubarius (pharyngeal end of the eustachian tube), and pharyngeal musculature (superior and middle constrictor, salpingopharyngeus, levator palatini).<sup>6,8</sup></p>
<h3>Pharyngeal Mucosal Infections</h3>
<p>Many aerodigestive tract infections start in the pharyngeal mucosal space. Infections in this space can demonstrate a wide array of signs and symptoms including pharyngitis, tonsillitis, suppuration, and tonsillar abscess.<sup>1</sup> In general, these are polymicrobial infections with diverse aerobic and anaerobic flora. Nonetheless, <em>Fusobacterium necrophorum</em> and Streptococcus group A are among the most prevalent pathogens.<sup>9</sup> Tonsillitis is a clinical diagnosis, but as inflammation progresses, suppuration and phlegmon can develop. Imaging findings consist of diffusely enlarged tonsils, abscess formation, and peritonsillar inflammation (<strong>Figure 2</strong>). Tonsillar abscess typically originates between the tonsillar capsule and pillar (<strong>Figure 3</strong>). Distinction between phlegmon and abscess is important as it will dictate clinical management. If an abscess is present, aspiration is the standard of care.<sup>10</sup></p>
<h2>Submandibular/Sublingual Space</h2>
<p>The submandibular space corresponds to the compartment at the floor of the mouth (<strong>Figure 1</strong>). Contiguous across the midline ventrally, it is outlined anteriorly by the arch of the mandible and posteriorly by the submandibular glands. Its superior margin, the mucosa of the floor of the mouth, can be appreciated on physical examination. Caudally it is bounded by insertion of the SLDCF into the hyoid bone. The space is subdivided into two compartments by the mylohyoid muscle: the sublingual (superiorly) and submandibular (inferiorly). The sublingual compartment contains the sublingual glands, the duct and deep portion of the submandibular gland, the lingual vessels, and the glossal/hypoglossal nerves. The submaxillary space contains the superficial portion of the submandibular gland. The compartments communicate at the posterior margin of the mylohyoid, which accounts for the &ldquo;diving&rdquo; appearance of a ruptured ranula. In 77% of cases, the compartments may communicate through a defect in the mylohyoid muscle (a boutonniere), which may present as a palpable lump of a herniated sublingual gland.<sup>5,11</sup></p>
<h2>Parotid Space</h2>
<p>The parotid space (PS) contains the parotid gland, which is bifurcated by the facial nerve into superficial and deep lobes. On routine CT or MRI, a more conspicuous anatomic landmark is the retromandibular vein, which lies just medial to the facial nerve. Another landmark is the external carotid artery, located immediately medial to the retromandibular vein. The SLDCF surrounds the parotid space (<strong>Figure 1</strong>). Craniocaudally, the parotid space extends from the external auditory canal/mastoid tip to the parotid tail, just below the mandibular angle. The parotid tail lies between the platysma and sternocleidomastoid muscles. The poststyloid (retrostyloid) parapharyngeal space is posteromedial to the parotid space, separated by the digastric muscle posterior belly. The parapharyngeal space lies medial to the parotid space. The contents of the parotid space include the parotid gland, facial nerve, retromandibular vein, external carotid artery branches, lymph nodes, and parotid (Stensen) ducts.<sup>8</sup></p>
<p>A common anatomic variant is the parotid gland accessory third lobe, superficial to the masseter muscle. The parotid duct courses along the margin of the masseter muscle, entering the buccinator muscle at the level of the second maxillary molar. A normal duct is too small for routine identification on imaging. Intraparotid lymph nodes are routinely seen because parotid gland encapsulation occurs after nodal chain development.<sup>6</sup></p>
<h3>Salivary Gland Infections</h3>
<p>Acute sialadenitis may be viral, bacterial or calculus induced. Patients are typically ill with acute pain exacerbated by food. Leukocytosis is usually present.<sup>1,2</sup> When dealing with salivary gland infections it is fundamental to consider symptom chronicity and laterality. This approach will help the interpreting radiologist distinguish between isolated and systemic pathologies and will also aid in selecting the imaging modality of choice. For example, a sialolith may be better depicted by CT than MRI. Bacterial infections are more common in adults following recent surgery with intubation and dehydration as predisposing factors (<strong>Figure 4</strong>). <em>Staphylococcus aureus</em> is amongst common pathogens in adults, whereas Paramyxovirus (mumps) is the most common culprit in the pediatric population, but other viruses such as adenovirus and parainfluenza are also common pathogens. When multiple lesions are within the parotid gland, HIV infection should also be considered as a possible diagnosis.<sup>12</sup></p>
<p>Imaging will demonstrate an enlarged gland with periglandular inflammatory change. A dilated duct may be present in cases of calculus sialadenitis (<strong>Figure 5</strong>). Chronic sialadenitis may present with a firm and painless gland with fatty atrophy. Abscess formation constitutes a late complication with the parotid gland being the most common location. Viral sialadenitis is a systemic process, usually bilateral, and may involve more than one group of salivary glands.<sup>2</sup></p>
<h2>Retropharyngeal (Retrovisceral) Space</h2>
<p>The retropharyngeal or retrovisceral space (RS) spans the suprahyoid and infrahyoid neck as contiguous retropharyngeal and retroesophageal spaces (<strong>Figure 1</strong>). The region extends from the skull base caudally to the mediastinal fusion of the anterior buccopharyngeal and posterior alar fascia (most commonly near the level of the tracheal bifurcation). Laterally, a band of fascia known as the <em>cloison sagittale</em> separates it from the parapharyngeal space. The RS and pretracheal spaces communicate around the esophagus between the thyroid cartilage and inferior thyroidal artery.<sup>5,12</sup></p>
<h3>Retropharyngeal Infections</h3>
<p>Retropharyngeal infections constitute a deep neck infection allowing for potentially lethal complications. The suprahyoid RS contains lymph nodes and fat, whereas the infrahyoid RS only contains fat. Infections are secondary to direct spread or from direct inoculation in the setting of penetrating trauma. Patients can present with different symptoms depending on where the process arises. Infections usually begin in the pharynx, paranasal sinuses, middle ear, or prevertebral space. Contrast-enhanced CT of the neck is usually the imaging modality of choice. Findings vary from low attenuation effusion of the RS to phlegmon and abscess formation. Impaired lymphoid drainage or excess lymphoid production will lead to local edema and nodal enlargement. Suppurative nodes and retropharyngeal abscess are at times used interchangeably. However, distinction between the two is important because it will dictate clinical management. Suppurative nodes consist of enlarged nodes with internal necrosis, with pus formation contained within the thick enhancing node capsule (<strong>Figure 6</strong>).<sup>13,14</sup> A retropharyngeal abscess usually manifests as a low attenuation fluid collection that will result in anterior displacement of the of the posterior pharyngeal wall from the prevertebral muscles. Retropharyngeal abscess does not typically exhibit a thick enhancing wall.<sup>15</sup></p>
<h2>Posterior Cervical Space</h2>
<p>The posterior cervical space corresponds to the posterior triangle of the neck outlined by the sternocleidomastoid anteriorly and the trapezius posteriorly. The medial fascial boundary is demarcated by the DLDCF as it curves around the paraspinal muscles of the prevertebral space from the spinous processes/nuchal ligaments posteriorly, to the transverse processes of the cervical vertebra anteriorly (<strong>Figure 1</strong>). Although separate from this compartment, the posterior triangle also encompasses a space containing the spinal accessory nerve and its lymph node chain. Lymphadenopathy in this chain will result in a characteristic anterior displacement of the carotid sheath, which lies ventrally.</p>
<h3>Pre- and Perivertebral Infections</h3>
<p>The bulk of the pre- and perivertebral space (PVS) is comprised of muscles and osseous structures. Infection is common and usually occurs from direct inoculation after trauma or surgery, direct extension, or hematogenous spread. Predisposing risk factors include intravenous drug use and immunocompromised status. Symptoms vary, including neck pain, focal tenderness, and myelopathy if epidural involvement is present. <em>Staphylococcus aureus</em> is one of the most commonly isolated pathogens. Contrast-enhanced CT and MRI are complementary when evaluating the PVS. Imaging findings include pre- or perivertebral fluid, myositis, endplate destruction (discitis/osteomyelitis and presence of hardware construct). Edema in this space will displace the longus capiti muscles, a helpful clue that will differentiate from a process arising in the RS (<strong>Figure 7</strong>). The DLDCF confines the infection so that it preferentially extends into the epidural space.<sup>16,17</sup> Nodal involvement is common.<sup>14</sup></p>
<h2>Masticator Space</h2>
<p>The masticator space (MS) consists of paired spaces on each side of the face and is bounded by the SLDCF. The SLDCF splits in two layers at the lower border of the mandible. The superficial layer encloses the masseter muscle extending over the zygomatic arch and attaches to the lateral orbital wall. The deep layer extends medial to the medial pterygoid muscle and attaches to the skull base medial to the foramen ovale. These two layers fuse along the borders of the mandibular ramus.<sup>5,15</sup> The MS comprises masticator muscles (pterygoid, masseter and temporalis) and the posterior mandibular ramus.<sup>19</sup></p>
<h3>Masticator Infections</h3>
<p>Clinical evaluation of the masticator space is limited. Patients may complain of trismus mimicking temporomandibular joint disease. Most MS infections are the result of direct spread of advanced odontogenic infections (<strong>Figure 8</strong>). Several pathways of spread had been proposed, which include a cortical break along the buccal aspect of the maxillary bone with propagation along the medial pterygoid muscle fibers. Secondary extension is directed superiorly along interlaced muscle fibers and vertical orientation of the cervical fascia.<sup>20</sup> Imaging findings include edema and muscle stranding with occasionally phlegmon/abscess formation, classically situated adjacent to the mandibular ramus.<sup>2</sup></p>
<h2>Unique Entities</h2>
<h3>Lemierre Syndrome</h3>
<p>Acute oropharyngeal infection can cause septic thrombophlebitis of the internal jugular vein. This process is almost exclusively caused by <em>Fusobacterium necrophorum</em>. Infection occurs after lateral spread from the lateral pharyngeal space. Neck swelling and tenderness are the hallmark symptoms (<strong>Figure 9</strong>). Pulmonary nodules are also found as the venous system serves as a route of metastatic spread. Contrast-enhanced CT of the neck is the modality of choice and will demonstrate thrombosis of the internal jugular vein and thrombophlebitis.<sup>2</sup></p>
<h3>Carotidynia or Fay Syndrome</h3>
<p>This is a poorly understood syndrome manifested by unilateral neck pain and increased pulsation in the affected side.<sup>21</sup> Imaging findings consist of amorphous soft tissue or stranding replacing the fat surrounding the carotid artery without luminal narrowing. Patients usually complain of neck pain with tenderness to palpation over the carotid bifurcation (<strong>Figure 10</strong>).<sup>22</sup></p>
<h2>Summary</h2>
<p>Imaging plays an important role in the evaluation of neck infections and CT and/or MR imaging is commonly obtained in the emergency department. Clinical presentations vary based upon the neck compartment in which each entity arises. Knowledge of the imaging patterns and potential complications of various infectious processes will allow the radiologist to provide an accurate and prompt diagnosis, evaluate for potential complications, and ensure optimal treatment.</p>
<h2>References</h2>
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<li>Maroldi R, Farina D, Ravanelli M, Lombardi D, Nicolai P. Emergency imaging assessment of deep neck space infections. Semin Ultrasound CT and MRI 2012;33(5):432-442. doi:10.1053/j.sult.2012.06.008</li>
<li>King KM. Head and neck imaging. 3rd ed, 2 vols. Radiology 1997;204(1):220-220. doi:10.1148/radiology.204.1.220</li>
<li>Sutcliffe P, Lasrado S. Anatomy, head and neck, deep cervical neck facia. In: StatPearls. StatPearls Publishing; 2019. http://www.ncbi.nlm.nih.gov/books/NBK541091/. Accessed December 6, 2019.</li>
<li>Guidera AK, Dawes PJD, Fong A, Stringer MD. Head and neck fascia and compartments: no space for spaces. Head Neck 2014;36(7):1058-1068. doi:10.1002/hed.23442</li>
<li>Gamss C, Gupta A, Chazen JL, Phillips CD. Imaging evaluation of the suprahyoid neck. Radiol Clin North Am 2015;53(1):133-144. doi:10.1016/j.rcl.2014.09.009</li>
<li>Weber AL, Siciliano A. CT and MR imaging evaluation of neck infections with clinical correlations. Radiol Clin North Am 2000;38(5):941-968. doi:10.1016/S0033-8389(05)70214-1</li>
<li>Rubin JA, Wesolowski JR. Neck MR imaging anatomy. Magn Reson Imaging Clin N Am 2011;19(3):457-473, vii. doi:10.1016/j.mric.2011.05.003</li>
<li>Klug TE, Henriksen J-J, Fuursted K, Ovesen T. Significant pathogens in peritonsillar abscesses. Eur J Clin Microbiol Infect Dis 2011;30(5):619-627. doi:10.1007/s10096-010-1130-9</li>
<li>Ludwig BJ, Foster BR, Saito N, Nadgir RN, Castro-Aragon I, Sakai O. Diagnostic imaging in nontraumatic pediatric head and neck emergencies. RadioGraphics 2010;30(3):781-799. doi:10.1148/rg.303095156</li>
<li>La&rsquo;Porte SJ, Juttla JK, Lingam RK. Imaging the floor of the mouth and the sublingual space. RadioGraphics. 2011;31(5):1215-1230. doi:10.1148/rg.315105062</li>
<li>Parker GD, Harnsberger HR. Radiologic evaluation of the normal and diseased posterior cervical space. Am J Roentgenol 1991;157(1):161-165. doi:10.2214/ajr.157.1.2048512</li>
<li>Shefelbine SE, Mancuso AA, Gajewski BJ, Ojiri H, Stringer S, Sedwick JD. Pediatric retropharyngeal lymphadenitis: differentiation from retropharyngeal abscess and treatment implications. Otolaryngol Head Neck Surg 2007;136(2):182-188. doi:10.1016/j.otohns.2006.03.002</li>
<li>Hoang JK, Branstetter BF, Eastwood JD, Glastonbury CM. Multiplanar CT and MRI of collections in the retropharyngeal space: is it an abscess? Am J Roentgenol 2011;196(4):W426-432. doi:10.2214/AJR.10.5116</li>
<li>Bou-Assaly W, Mckellop J, Mukherji S. Computed tomography imaging of acute neck inflammatory processes. World J Radiol 2010;2(3):91-96. doi:10.4329/wjr.v2.i3.91</li>
<li>Mills MK, Shah LM. Imaging of the perivertebral space. Radiol Clin North Am 2015;53(1):163-180. doi:10.1016/j.rcl.2014.09.008</li>
<li>Capps EF, Kinsella JJ, Gupta M, Bhatki AM, Opatowsky MJ. Emergency imaging assessment of acute, nontraumatic conditions of the head and neck. RadioGraphics 2010;30(5):1335-1352. doi:10.1148/rg.305105040</li>
<li>Wei Y, Xiao J, Zou L. Masticator space: CT and MRI of secondary tumor spread. Am J Roentgenol 2007;189(2):488-497.</li>
<li>Fernandes T, Lobo JC, Castro R, Oliveira MI, Som PM. Anatomy and pathology of the masticator space. Insights Imaging 2013;4(5):605-616. doi:10.1007/s13244-013-0266-4</li>
<li>Schuknecht B, Stergiou G, Graetz K. Masticator space abscess derived from odontogenic infection: imaging manifestation and pathways of extension depicted by CT and MR in 30 patients. Eur Radiol 2008;18(9):1972-1979. doi:10.1007/s00330-008-0946-5</li>
<li>Santarosa C, Stefanelli S, Sztajzel R, Mundada P, Becker M. Carotidynia: a rare diagnosis for unilateral neck pain revealed by cross-sectional imaging. Case Rep Radiol 2017;2017. doi:10.1155/2017/7086854</li>
<li>Lecler A, Obadia M, Savatovsky J, et al. TIPIC Syndrome: beyond the myth of carotidynia, a new distinct unclassified entity. Am J Neuroradiol 2017;38(7):1391-1398. doi:10.3174/ajnr.A5214</li>
</ol>9872Oncologic Emergencies of the Abdomen and Pelvis2020-04-14T09:40:08-04:002020-04-14T09:40:08-04:00Evan Ruppell, D.O., Hemang Kotecha, D.O., Lacey McIntosh, D.O.<p>Many of the more lethal malignancies originate from viscera in the abdomen and pelvis including tumors of the prostate, pancreas, liver, and colon/rectum.<sup>1</sup> In the ongoing work to improve patient survival, imagers must be cognizant of oncologic emergencies. These are defined as acute, potentially life-threatening events that develop as effects of cancer or its treatment. The most common oncologic emergencies relate to the gastrointestinal system and have a high association with mortality.<sup>2,3</sup> Oncologic emergencies can occur at any point during disease and may be the initial presenting manifestation. These emergencies are not limited to malignancies, as pathologically benign tumors may also present emergently causing life-threatening bowel, biliary, or ureteral obstruction.<sup>4</sup> The imager&rsquo;s role is critical as prompt diagnosis increases the likelihood of a positive outcome.</p>
<p>The imaging manifestations of oncologic emergencies can be categorized into distinct patterns affecting the vascular, biliary, bowel, and genitourinary systems. CT will be emphasized as the modality of choice for most oncologic emergencies; however, there are often ancillary roles for ultrasound for initial screening, as well as nuclear medicine studies and MRI for further characterizing previously detected abnormalities. In addition to imaging findings, common clinical presentations will be discussed, as correlation with signs and symptoms adds value to the radiologist&rsquo;s report and facilitates future imaging.</p>
<h2>Vascular</h2>
<h3>Hemoperitoneum</h3>
<p>Spontaneous hemoperitoneum can occur in hypervascular tumors such as hepatocellular carcinoma (HCC), angiosarcoma, pancreatic solid pseudopapillary tumor (SPT), and neuroendocrine tumors. In high HCC-prevalent regions of Asia and Africa, lifetime incidence of spontaneous hemorrhage from HCC can be as high as 14%.<sup>5</sup> Rarely, hematogenous malignancies can present with intraperitoneal hemorrhage secondary to coagulopathy. Patients often present with diffuse abdominal pain due to peritoneal inflammation by blood. Larger volume hemorrhages result in hypovolemia, with nausea, hypotension, tachycardia, and eventually shock. Laboratory values may show drop in hematocrit; however, values are often normal. CT is, therefore, critical in diagnosis.</p>
<p>Imaging will demonstrate variable attenuation of blood products depending on acuity. Anemia or dilution by ascites may also decrease attenuation, with typical density of 35 to 45 HU.<sup>6</sup> While presence of hemoperitoneum can be detected by noncontrast CT, localizing the source of hemorrhage is facilitated by intravenous contrast administration (<strong>Figure 1</strong>). Most abdominopelvic CT imaging in the setting of acute abdominal pain will be performed in the portal venous phase, which can identify the presence of hemoperitoneum, as well as demonstrate the sentinel clot sign, which may help localize the likely site of active bleeding. Clotted blood is of higher attenuation (45 to 70 HU), which will stand out against the background of nonclotted blood.&nbsp;Imaging in the arterial phase with CT angiography (CTA) can demonstrate and localize active arterial extravasation and guide further treatment by surgical or interventional radiology teams.</p>
<p>Trauma may complicate interpretation because certain tumors are more vulnerable to injury than adjacent normal parenchyma. For instance, a small liver HCC could potentially hemorrhage after minor blunt trauma and be misinterpreted as a laceration. A spleen that is enlarged due to lymphoma involvement is similarly at increased risk for rupture.<sup>7</sup> Careful review of history and ancillary findings aids appropriate diagnosis.</p>
<p>Immediate treatment consists of intravenous infusion of fluids and blood products to improve hemodynamic stability. Correction of coagulopathy is also attempted to the extent possible with platelets and clotting factors. Surgery or targeted embolization should also be considered for focal masses with life-threatening hemorrhage.</p>
<h3>Acute Gastrointestinal Hemorrhage</h3>
<p>Malignancy is an uncommon cause of gastrointestinal (GI) bleeding, comprising approximately 7% of lower GI bleeds.<sup>8</sup> Focal hemorrhage due to cancer in the bowel is almost exclusively due to primary adenocarcinoma, which causes diffuse mucosal ulceration and/or erosion into adjacent vessels. Rare hemorrhages caused by direct vascular invasion by other aggressive abdominal tumors (such as HCC or pancreatic adenocarcinoma) have been reported.<sup>9</sup> Hemorrhage over a long segment of bowel may also occur as a consequence of treatment for hematologic disease. Twenty percent of patients with graft vs host disease (GVHD) after allogenic marrow transplant will suffer from diffuse or long segment moderate-severe GI bleeding, usually from the small bowel.<sup>10</sup></p>
<p>Gastrointestinal hemorrhage secondary to cancer is frequently low volume and not radiographically evident.<sup>11</sup> A hemorrhage rate of at least 0.35 ml/min is typically required for CTA detection, which will demonstrate focal hyperdense contrast extravasation within the bowel lumen.<sup>12</sup> A circumferential or focal mass in the bowel may be detected; however, these are often small. When utilizing CTA to evaluate for acute GI bleed, it is imperative that oral contrast not be administered, as it will obscure a typically small volume of intra-arterial contrast extravasating into the lumen. GVHD disease usually results in hyperdense fluid in the bowel due to diffuse oozing of blood. It is accompanied by long-segment small bowel wall thickening and smooth central enhancement (<strong>Figure 2</strong>).</p>
<p>As an alternative to CTA, Tc-99m red blood cell (RBC) scintigraphy is more sensitive for bleeding, requiring a rate of at least 0.2 ml/min to detect active hemorrhage.<sup>12</sup> The longer imaging time of scintigraphy also improves the detection of intermittent bleeds. Imaging of an active bleed will demonstrate accumulation of a radiotracer in the bowel outside of the intravascular compartment (<strong>Figure 3</strong>). Continued imaging may show a radiotracer in transit along the course of the bowel by peristalsis. Despite the increased sensitivity of scintigraphy, CTA is preferred at most institutions because of more accurate localization and improved detection of soft-tissue findings. Of note, some limitations on nuclear medicine exams may improve with hybrid SPECT/CT imaging.</p>
<p>Catheter-directed angiography requires a rate of at least 1 ml/min for diagnostic localization of an active hemorrhage but has the added advantage of allowing concurrent therapeutic embolization.<sup>12</sup> This modality is most useful for cases of massive bleeding (the requirement of transfusion of at least 4 units of blood over 24 hours or hypotension with systolic blood pressure &lt; 90 mm Hg) or when endoscopic management has failed.<sup>13</sup> Both scintigraphy and CTA are useful for guiding interventional radiology, endoscopic, and surgical procedures.</p>
<h3>Acute Venous Thrombosis and Thromboembolic Events</h3>
<p>Approximately 3% of all cases of acute mesenteric thrombosis affect the veins, and malignancy is found in a subset of 4% to 16% of these cases (most commonly myeloproliferative disorders).<sup>14,15</sup> Mesenteric thrombosis is much less common than deep venous thrombosis and pulmonary embolism, but shares the common mechanism of over-expression of procoagulant factors by both tumor cells and noncancerous tissue. The classic clinical presentation is pain out of proportion to physical examination findings, which begin with subtle distension and blood in the stool.</p>
<p>Findings are occasionally difficult to identify on CT, with retrospective studies indicating at least 90% accuracy in diagnosis of venous mesenteric thrombosis.<sup>14 </sup>On portal venous phase contrast-enhanced CT, the filling defect in the mesenteric vasculature appears as a central hypodensity with enhancement of the wall of the affected vessel. Other potential associated findings include portal venous thrombosis and those of intestinal infarction, typified by bowel hypoenhancement, wall thickening, and pneumatosis intestinalis. Although it is rarely considered, catheter-directed mesenteric angiography can be performed in indeterminate cases and would demonstrate a filling defect with late opacification of the proximal vein.<sup>16</sup></p>
<p>Treatment with anti-angiogenic agents has also been shown to result in arterial and/or venous thrombotic events (<strong>Figure 4</strong>).<sup>17</sup> This is most common in patients treated with bevacizumab for metastatic colorectal cancer, with relative risks of 1.3 for venous and 1.6 for arterial thromboembolic events.<sup>18</sup> The exact mechanism by which thrombosis occurs is not clear, but theories propose that inhibition of VEGF increases vascular inflammation and viscosity/platelet aggregation.</p>
<p>Overall patient survival is better for venous ischemia compared to arterial ischemia but will depend on the specific course of the patient&rsquo;s cancer.<sup>19</sup> Those with limited disease can be treated with systemic anticoagulation and bowel rest, while emergent surgical resection is indicated when bowel infarction has occurred.</p>
<h2>Pancreaticobiliary</h2>
<h3>Obstruction</h3>
<p>Pancreatic, ampullary, duodenal, bile duct, and hepatic tumors can result in pancreaticobiliary obstruction, usually by direct invasion or compression of the ducts. Typically, common bile duct (CBD) obstruction is caused by pancreatic ductal adenocarcinoma, followed by invasive cholangiocarcinoma and gallbladder carcinoma. However, any sufficiently large tumor can obstruct ducts by mass effect (<strong>Figure 5</strong>). Fifty-five percent of patients with pancreatic ductal adenocarcinoma will present with jaundice due to conjugated hyperbilirubinemia, which progressively worsens as the obstruction becomes complete.<sup>20</sup> Although the classically suspicious symptom for cancer is painless jaundice, 79% of patients with pancreatic ductal adenocarcinoma present with epigastric pain. Left untreated, obstruction may lead to cholangitis.</p>
<p>The initial imaging test ordered to evaluate obstruction will depend on clinical suspicion. CT is comparable to endoscopic retrograde cholangiopancreatography (ERCP) in establishing the presence of malignant extrahepatic obstruction. In addition to being noninvasive, CT can show ancillary findings such as metastases. Ultrasound is significantly worse for diagnosis (sensitivity of 57%); however, due to its low cost it may be used as the initial study when benign disease is suspected.<sup>21</sup> When no obvious mass is identified, MR cholangiopancreatography (MRCP) should be considered.</p>
<p>Strict size criteria for diagnosing CBD dilation are controversial; however, a simple formula of 6 mm plus 1 mm for each decade after age 60 is generally accepted.<sup>22</sup> The size of the common bile duct may also be increased after cholecystectomy, with potential normal dilation of up to 10 mm.<sup>23</sup> Intrahepatic ductal dilation can be defined as ductal size &gt; 2 mm or &gt; 40% of the adjacent portal vein.<sup>24</sup> Dilation of both the intra- and extrahepatic ducts is more suspicious for obstructing malignancy than dilation of the extrahepatic ducts alone. Dilation of intrahepatic ducts alone may suggest a hilar or intrahepatic malignancy.</p>
<p>Endoscopic stenting may be initially used as a bridge to surgery, or for palliation in patients with unresectable disease. Stents do not interfere with the ability to perform subsequent pancreaticoduodenectomy. Strictures that cannot be traversed with an internal drain require percutaneous external biliary drain placement to decompress the biliary ducts.<sup>25</sup></p>
<h3>Cholecystitis</h3>
<p>Gallbladder carcinoma is a rare malignancy that rarely causes acute cholecystitis. Adenocarcinoma represents 90% of cases, with the remainder consisting of squamous, adenosquamous, lymphoma, small cell, and sarcoma malignancies. The rate of incidental gallbladder carcinoma in patients undergoing cholecystectomy for acute cholecystitis in the US is approximately 0.5% but may be as high as 2.3% in East Asia.<sup>26</sup> As symptoms are related to cystic duct obstruction by the tumor, they closely mimic symptoms of calculous cholecystitis, with acute right upper quadrant pain, fever, and Murphy&rsquo;s sign.</p>
<p>Gallbladder carcinoma is usually advanced at presentation and has a propensity for invading the adjacent liver (<strong>Figure 6</strong>). Many cases present with metastases or bulky porta hepatis and para-aortic lymphadenopathy, with only 25% of these treated with potentially curative resection.<sup>27</sup> A minority of patients with gallbladder carcinoma have subtle findings, which can make prospectively differentiating acute cholecystitis from early gallbladder cancer difficult. A small study has demonstrated that elevated C-reactive protein level and less regional fat stranding are reliable indicators of gallbladder cancer, while cholelithiasis and leukocytosis are not.<sup>28</sup> Irregular wall thickening was useful when present, but only 20% of cancers were polypoid in morphology with the rest infiltrative. The presence of cholelithiasis is not a useful discriminating factor because most patients with gallbladder cancer have gallstones&mdash;in fact, larger stones and longer duration of cholelithiasis are both major risk factors for developing gallbladder carcinoma.<sup>29</sup> While white blood cell (WBC) counts tend to be higher in acute cholecystitis by itself, WBC counts are also usually abnormal in gallbladder carcinoma with acute cholecystitis due to acute inflammation.<sup>30</sup></p>
<p>Cholecystitis in the setting of gallbladder malignancy may be addressed definitively by surgery in certain circumstances. Simple laparoscopic cholecystectomy is considered appropriate for T1a disease, with cure rates ranging from 85% to 100% if negative margins are attained. Only retrospective studies are available as to outcomes for more advanced disease; however, most show that more radical surgery portends better outcomes.<sup>31</sup>&nbsp;An extended cholecystectomy at a minimum involves resection of a rim of hepatic segments IVb and V. T4 disease, which invades the main portal vein, hepatic artery, or multiple extrahepatic organs, is unresectable and best suited to palliative care such as cholecystostomy.</p>
<p>Cholecystitis has also been reported in a small number of cases as a treatment-related side effect from immune checkpoint inhibitor therapy. In contrast to cystic duct obstruction by invasion or compression, the cause is believed to be an autoimmune-related inflammatory state in the gallbladder. These cases were seen in association with drugs targeted to the PD-L1 / PD-1 and CTLA-4 pathways. The role of steroids has not yet been defined, so these cases are managed similarly to cases of typical cholecystitis.<sup>32</sup></p>
<h2>Bowel</h2>
<h3>Obstruction</h3>
<p>Malignancy is a common cause of obstruction of both the small and large bowel. Approximately 20% of small bowel obstructions are due to tumors, predominantly metastases from ovarian, colonic, pancreatic, and gastric neoplasms.<sup>33</sup> Of primary small bowel tumors resulting in obstruction, gastrointestinal stromal tumors (GIST) are most common, followed by lymphoma and adenocarcinoma.<sup>34</sup> In the large bowel, roughly 70% of all obstructions are due to neoplasm, with almost one-fifth of all cases of colon cancer complicated by obstruction at some point. Usually this is due to locally advanced but resectable primary adenocarcinoma. A minority of bowel obstructions occur with lymphoma and noncolonic neoplasms such as pancreatic and ovarian cancer.<sup>35</sup> Patients with acute obstruction will present with abdominal distension, signs of dehydration, and a tympanic abdomen. Often the slow growth of tumors leads to an insidious onset with postprandial discomfort and nausea leading up to acute complete obstruction.&nbsp;</p>
<p>Radiography of acute small bowel obstruction demonstrates dilated bowel loops with air-fluid levels; however, contrast-enhanced CT has become the imaging modality of choice.<sup>36</sup> CT better shows the location, severity, etiology, and complications of obstruction. Classically, the tumor is located in the ileum and results in enhancing short segment thickening of the bowel wall, with upstream dilation. Masses often serve as a lead point for intussusception, which produces a bowel-within-bowel appearance. The small bowel feces sign (<strong>Figure 7</strong>) appears as gas and particulate matter just proximal to the mass, pointing to the site of obstruction.<sup>37</sup>&nbsp;</p>
<p>In the large bowel, the classic obstructing tumor is in the rectosigmoid colon, the same location for the most common nonmalignant source of large bowel obstruction, sigmoid volvulus. Because of the colon&rsquo;s greater capacity to distend, adenocarcinoma classically produces a circumferential &ldquo;apple core&rdquo; lesion (<strong>Figure 8</strong>). Upstream dilation varies but can measure &gt; 8 cm proximal to the transition point.<sup>38</sup></p>
<p>Emergent surgery should be performed in cases where perforation or ischemia is evident, manifested by pneumatosis intestinalis or portal venous gas.<sup>39</sup> In the large bowel, flexible sigmoidoscopy, often with endoscopic stenting (<strong>Figure 9</strong>) appears reasonably successful for preoperative decompression or palliation.<sup>40</sup></p>
<h3>Ischemia, Perforation, and Fistula</h3>
<p>These rare GI oncologic complications can occur spontaneously but are increasingly likely to be related to targeted drug and radiation treatments. The complications of ischemia, perforation, and fistula share several common suspected mechanisms related to pressure necrosis, mural infiltration by malignant cells, and/or inflammation due to radiation and chemotherapy.<sup>41</sup> Patients will usually present with abdominal pain, nausea, and fever. Of note, as many as 12.5% of patients with tumor-bowel fistulas will be asymptomatic at diagnosis. Intravenous and oral contrast-enhanced CT is the imaging study of choice.</p>
<p>The most common causes of tumor-bowel fistulas (TBF) are bulky cervical, ovarian, and colon cancers. Primary small bowel tumors and lymphoma are rarely associated. Tumor size is the primary risk factor, with case studies reporting 8 to 26 cm.<sup>42</sup> Another important risk factor is chemoradiotherapy. A case study of 2096 cervical cancers found that all 38 patients who developed TBFs had undergone prior radiation therapy.<sup>43</sup> TBF should be suspected on imaging when gas is present within a tumor; however, gas may also be a sign of bacterial infection. In unclear cases, the administration of oral contrast allows for a more confident diagnosis when contrast is seen extending into the tumor. A tract between the tumor and nearby bowel can often be appreciated on reformats (<strong>Figure 10</strong>).</p>
<p>The risk of tumor-related perforation is highest in ovarian, pancreatic, colon, and rectal cancers. Molecular targeted therapy with antiangiogenic drugs is particularly associated with perforation, and to a lesser extent, fistula. For instance, treatment with bevacizumab (a monoclonal antibody which inhibits VEGF-A) carries a risk of bowel perforation between 1% and 4%.<sup>44</sup> On imaging, gas and fluid are usually proximal to the site of perforation (<strong>Figure 11</strong>). Large bowel perforations can result in massive pneumoperitoneum, whereas small bowel perforations can be more difficult to detect. In some cases, the gas remains closely localized to the site of perforation due to containment by inflammatory reaction.</p>
<p>Early discontinuation of treatment is important for initial treatment of both TBF and perforation, as stopping molecular targeted therapy is associated with reversal of pneumatosis.<sup>45</sup> Definitive management requires surgical resection, but conservative management can be attempted in the absence of peritonitis or sepsis.</p>
<h2>Genitourinary</h2>
<h3>Urinary Tract Obstruction</h3>
<p>In addition to urothelial cell carcinoma (UCC), urinary tract obstruction occurs often in patients with a variety of malignancies involving the retroperitoneum and pelvis including colon, ovary, and prostate neoplasms causing direct invasion or compression. Malignant urinary obstruction is an ominous development, with a median survival time of 3 months.<sup>46</sup> Lymphoma/lymphadenopathy less commonly results in obstruction (<strong>Figure 12</strong>). Primary urothelial cell carcinoma (UCC) of the ureter is exceedingly rare, occurring approximately 100 times less frequently than UCC of the bladder. In addition to pain, patients are at high risk for developing sepsis related to obstruction and may also develop hypertension from electrolyte and water retention. Symptoms are variable depending on the acuity of obstruction. When due to unilateral external compression, patients are often initially asymptomatic because of the slow progression of disease.</p>
<p>In order of increasing preference, ultrasound, CT without contrast, contrast-enhanced CT, and CT/MR urography can be used to image malignant obstruction. Noncontrast CT and ultrasound are often performed in the emergent setting because of concurrent acute renal failure, prohibiting the use of intravenous contrast. While any portion of the collecting system can be involved, the distal third of the ureter is a frequent site (<strong>Figure 13</strong>).<sup>47</sup> Proximally, the collecting system will be dilated with the kidney demonstrating a delayed nephrogram on contrast-enhanced CT. A delayed nephrogram (<strong>Figure 14</strong>) appears as reduction of the normal renal parenchymal enhancement in the later phases of contrast excretion (the time point when venous-phase CT is performed). An infiltrating mass with adjacent fat stranding will often be seen in the renal pelvis or ureter in cases of UCC, occasionally appearing as an intrarenal mass when arising in a more proximal calyx. If no definite mass is identified, then irregular narrowing of the ureteral lumen can be a helpful sign.<sup>48</sup> Although infrequently performed by radiologists, retrograde pyelography may show contrast within the interstices of a UCC (stipple sign) and distal cupping of intraluminal tumor by contrast (goblet sign).</p>
<p>The three general categories of treatment for acute genitourinary obstruction are: palliation, treatment of extrinsic compression, and surgery. In the case of obstruction by metastasis, the usual approach is by palliation of symptoms with retrograde placement of a ureteric stent. If this cannot be accomplished, percutaneous nephrostomy catheter placement will relieve the obstruction but is more invasive and requires an external drainage bag. For extrinsic compression, treatment of the offending mass should resolve the obstruction; however, stents or nephrostomy tubes may be used as temporizing measures. Lastly, ureteral diversion surgeries can be considerered.<sup>47</sup></p>
<h3>Acute Adnexal Torsion</h3>
<p>Ovarian cysts and masses are the primary risk factors for adnexal torsion. Two case series of patients with ovarian torsion found that 31% to 46% had an ovarian mass, with most of the remainder having simple and hemorrhagic cysts.<sup>49,50</sup> Torsion is overwhelmingly more likely to occur in patients with benign masses. A potential explanation is that malignant masses preferentially develop a fixating desmoplastic reaction. Acute adnexal torsion is most likely to occur in patients of reproductive age. Pregnant patients are at particular risk, probably due to hypermobile ligaments.<sup>51</sup> Patients present with acute pelvic pain, nausea, and sometimes fever. The pain may be intermittent due to spontaneous detorsion and retorsion.</p>
<p>Initial investigation for torsion should be performed by ultrasound. The most reliable finding on ultrasound is an enlarged ovary, measuring &gt; 20 ml in volume or &gt; 4 cm in greatest dimension. The ovary may also demonstrate stromal edema and heterogeneity due to vascular outflow obstruction. An infrequent but specific sign for adnexal torsion is the twisted vascular pedicle (whirlpool sign). This manifests as a hyperechoic mass adjacent to the ovary with central hypoechoic vessels, sometimes with a beak-like interface. Unlike in the testes, arterial spectral Doppler waveforms may be preserved because of its dual-ovarian blood supply from uterine collaterals and the ovarian artery. Masses serving as lead points will have variable imaging appearance. Mature cystic teratoma is the most common mass seen in torsion, with benign serous cystadenoma slightly less likely (<strong>Figure 15</strong>).<sup>52</sup></p>
<p>While CT should not be performed as the primary modality in cases of suspected ovarian torsion, it may be the first line of imaging when symptoms and history are atypical. In addition to the ovary appearing enlarged and displaced, the uterus is often displaced toward the side of torsion. In less than one-third of cases, a twisting of the vascular pedicle in the affected adnexa can be visualized. Absent enhancement is a worrying sign for infarction of the ovary. MRI is not typically utilized in the emergent setting due to the ease of ultrasound but demonstrates a similar pattern of findings as described with CT, with T1 hypointense/T2 hyperintense edema.</p>
<p>Adnexal torsion, if not treated promptly, can lead to ovarian necrosis and infertility. Patients with an ovarian mass suspicious for malignancy require salpingo-oophorectomy, whereas benign cysts may be treated with cystectomy and detorsion/fixation of the ovary.<sup>53</sup></p>
<h2>Conclusion</h2>
<p>Oncologic emergencies of the abdomen and pelvis are life-threatening events of increasingly common incidence affecting the vascular, pancreaticobiliary, GI, and genitourinary systems. The radiologist should be able to quickly and accurately detect these findings. In patients with known cancer on treatment, clinical information should be integrated into interpretation to identify potential treatment-related emergencies.</p>
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</ol>9848Ultrasound and MRI Evaluation of the Lateral Ankle2020-01-24T11:27:25-05:002020-01-24T11:27:25-05:00Shefali Kanal, OMS3, Manal Saif, OMS4, Courtney Scher, D.O., Leah Davis, D.O.<p>Lateral ankle pain is a common clinical complaint and may result from an acute traumatic event, chronic repetitive trauma, impingement syndromes or alignment abnormalities resulting in altered biomechanics. Additional etiologies of ankle pain include synovial proliferative processes, inflammatory arthropathies and crystalline deposition disease. While these articular-based processes typically result in diffuse ankle pain, they may result in localized symptoms and should also be considered in patients with lateral ankle pain. The purpose of this article is to review the common anatomy and pathology of the lateral ankle and to discuss the common imaging findings seen on ultrasound (US) and MRI.</p>
<p>Acute lateral ankle injuries are common and include fractures, ligamentous sprains, and tendinous injuries. Lateral malleolar fractures may occur in isolation or in the setting of bi- or trimalleolar injuries. Lateral ligament complex injuries at the ankle are the most common reason for missed athletic participation, and occur during inversion when the ankle is in the relatively unstable, plantarflexed position.<sup>1</sup> Peroneal tendon injuries, including tendinosis, tears, or peroneal retinaculum injuries may occur in isolation but are common in the setting of lateral ligamentous injuries. Entrapment of peroneal tendons between fracture fragments may occur; tendons should be closely interrogated in patients with ankle fractures. In the acute setting, peroneal tendon injuries may be overlooked and underdiagnosed, as pain and laxity from ankle sprain often dominates the clinical picture.<sup>2,3</sup></p>
<p>Radiographs are the first line of imaging and should be obtained in weight-bearing, when possible, to evaluate alignment and integrity of the ankle mortise. While radiographs demonstrate most acute osseous injuries well, direct visualization of soft-tissue pathology often requires additional imaging. Both MRI and US can evaluate the ligaments and tendons of the lateral ankle. US has the advantage of assessing tendon motion during dynamic imaging and ligamentous integrity with applied stress; MRI is superior for the evaluation of intra-articular pathology and marrow signal abnormalities.</p>
<h2>Osseous Anatomy of the Ankle</h2>
<p>The ankle is composed of three main articulations: the tibiotalar (talocrural) joint, subtalar (talocalcaneal) joint, and the transverse tarsal (midtarsal joint) joint. The tibiotalar joint is a synovial hinge joint between the tibial plafond and talar dome and bears most of the load during weight-bearing. Its primary function is dorsiflexion and plantarflexion of the foot, although it aids in inversion/eversion and abduction/adduction as well.<sup>4</sup> The subtalar joint consists of three distinct calcaneal articulations and contributes to inversion and eversion of the foot. The transverse tarsal joint, also known as Chopart joint, is a compound joint that includes the talonavicular component of the talocalcaneonavicular joint as well as the calcaneocuboid joint, and assists with inversion and eversion. Collectively, the joints allow for complex motions such as supination (adduction, inversion and plantarflexion) and pronation (adduction, eversion and dorsiflexion) of the foot.<sup>4</sup></p>
<p>Acute trauma may result in fractures of the malleoli or fifth metatarsal, which are typically well visualized on radiographs. Fractures of the body or anterior process of the calcaneus, lateral talar process, lateral calcaneus, talar dome and lateral fibula from superior peroneal retinaculum avulsion injuries may be subtle or even occult on radiographs. Advanced imaging is performed in cases when there is a high clinical suspicion for occult fracture, or when more detailed evaluation of the soft tissues is clinically indicated.</p>
<p>Traumatic osteochondral injuries of the talar dome may result in a stable or unstable osteochondral lesion. Symptomatic osteochondral lesions often result in decreased range of motion and cause deep ankle pain with weight-bearing but patients may localize pain to the lateral ankle in the setting of lateral talar dome injuries. MRI is the modality of choice for evaluating osteochondral injuries as it can detect signs of instability, including a rim of fluid signal intensity surrounding the lesion, cysts underlying the lesion, discontinuities in the subchondral bone plate, or displaced intra-articular fragments (<strong>Figure 1</strong>).<sup>5</sup></p>
<h2>Ligaments of the Lateral Ankle</h2>
<p>The lateral ligaments of the ankle consist of the low ankle ligaments; the anterior talofibular, calcaneofibular and posterior talofibular ligaments; and the high ankle ligaments, the anterior and posterior tibiofibular, and interosseous ligaments (<strong>Figure 2</strong>). Lateral ankle ligament sprains account for 16% to 21% of sports-related injuries, with a predictable pattern of injury involving the weakest ligament, the anterior talofibular ligament (ATFL), followed by the calcaneofibular ligament (CFL), and finally the posterior talofibular ligament (PTFL).<sup>6</sup></p>
<h3>Low Ankle Ligaments</h3>
<p>The ATFL extends from the lateral malleolus to the talus and functions to prevent anterior displacement as well as excessive inversion and internal rotation of the talus on the tibia.<sup>7</sup> The ATFL is well visualized on MR as a hypointense band of tissue seen best on axial images (<strong>Figure 3A</strong>) and on US as a hypoechoic, linear structure seen best with the transducer in an oblique, short-axis plane (<strong>Figure 3B</strong>).</p>
<p>The CFL arises from the posterior aspect of the lateral malleolus, courses anteriorly on an oblique long axis, deep to the peroneal tendons, to insert on the lateral calcaneus. It functions to prevent excessive inversion and internal rotation as well as prevent excessive supination.<sup>7</sup> The CFL is stressed most in dorsiflexion and is the second most injured ligament during ankle injuries. On MRI, evaluation of sequential coronal or axial imaging is required to visualize its oblique course from the tip of the lateral malleolus to the lateral calcaneus (<strong>Figure 4A</strong>). On US, the CFL is well visualized on a long axis with the transducer in an oblique, short-axis plane (<strong>Figure 4B</strong>).</p>
<p>The PTFL runs from the posterior aspect of the lateral malleolus, with variable insertion on the posterolateral aspect of the talus, lateral talar process or os trigonum (if present) and protects the talocrural joint from excessive inversion and internal rotation.<sup>7</sup> It is the least injured low ankle ligament. The PTFL is typically well visualized on axial MR images but can also be seen well in cross-section on sagittal MR images (<strong>Figure 5</strong>), which may be helpful in assessing the architecture of the ligament in cases of questionable injury on axial images. As the PTFL is injured infrequently, it is not routinely imaged by US, but in cases of clinical suspicion, it can be seen well with the transducer in the short-axis plane over the posterolateral ankle.</p>
<p>Lateral ankle ligament sprains are classified on a three-point grading scale with grade I representing a stretch injury without tear, grade II a partial tear, and grade III a complete tear. Some authors classify low ankle sprains on an anatomic basis, with grade I injuries resulting in partial disruption of the ATFL, grade II involving partial disruption of the ATFL and CFL, and grade III demonstrating complete disruption of the ATFL or CFL.<sup>6</sup> With US or MR imaging, partial thickness injuries demonstrate heterogeneity and thickening of the ligament in the acute period, but are variable in appearance in the chronic setting, with thickening or thinning, ligamentous elongation, or wavy contour.<sup>6</sup></p>
<p>Complete tears of the ATFL result in a focal gap in the acute setting with adjacent hyperemia, ligament redundancy and disorganization of fibers on both MR and US (<strong>Figure 6</strong>). If varus stress is applied to the ankle during the US examination, gapping of the lateral clear space can be visualized.</p>
<h3>High Ankle Ligaments</h3>
<p>The distal tibia and fibula form a syndesmotic joint, composed of three major ligaments: the anterior tibiofibular, posterior tibiofibular, and interosseous (or transverse) tibiofibular ligament, which stabilize the high ankle.<sup>7</sup> Injuries to the high ankle ligaments occur in &lt; 11% of ankle sprains.<sup>8 </sup>The anterior tibiofibular ligament is trapezoidal in shape and runs from the anterior tubercle of the distal tibia obliquely to the anterior tubercle of the distal fibula. A thickened distal fascicle of the anterior tibiofibular ligament, termed the anterior inferior tibiofibular or Bassett&rsquo;s ligament, is present in some individuals and can be visualized on MRI.<sup>9,10</sup> Given its oblique orientation, the anterior tibiofibular ligament is difficult to visualize fully on a single MR image, but can be seen on axial MR at the level of the distal syndesmosis (<strong>Figure 7A</strong>). On US, the anterior tibiofibular ligament is easily visualized with the transducer in the short axis oblique position at the level of the distal syndesmosis (<strong>Figure 7B</strong>).</p>
<p>The posterior tibiofibular ligament is a triangular ligament that runs from the posterior tibial malleolus to the posterior tubercle of the fibula. It is extremely strong and formed by two independent components, superficial and deep, and has fibers that form a broad base at the tibial insertion.<sup>7</sup> The posterior tibiofibular ligament is the least injured high ankle ligament and can be assessed on axial MR images at the level of the distal syndesmosis. The interosseous ligament is at the far inferior aspect of the distal interosseous membrane and is formed by a dense mass of short fibers, which span the tibia to the fibula. Its contribution to ankle stability is controversial, with some claiming it is insignificant and others claiming it is the primary stabilizing bond between the tibia and fibula.<sup>11</sup></p>
<p>On initial radiographs, widening of the ankle mortise or distal tibiofibular syndesmosis as well as the presence of Weber B or Weber C lateral malleolus fractures should raise concern for high ankle ligamentous injury, as syndesmotic tears occur in approximately 50% of Weber B and in all Weber C fractures.<sup>8 </sup>Injuries to the high ankle ligaments are also graded on the standard three-point scale with grade I representing a stretch injury without tear, grade II a partial tear, and grade III a complete tear. On US and MRI, focal discontinuity of the ligament is consistent with a grade III, or complete, tear (<strong>Figure 8</strong>). Ligamentous thickening, laxity or irregular contour suggests a less severe grade II injury (<strong>Figure 9</strong>). Abnormal signal or echogenicity without structural abnormality is consistent with a grade I injury. Surrounding edema or hyperemia on Doppler US interrogation provides insight into acuity, as chronic injuries typically demonstrate irregular morphology without surrounding soft-tissue abnormalities.</p>
<h2>Tendons of the Lateral Ankle</h2>
<p>The peroneus longus muscle originates from the head of the fibula, and the peroneus brevis muscle originates from the mid-distal lateral fibula and the intermuscular septum. They both course distally in the lateral compartment of the lower leg. At the ankle, the tendons course through the retromalleolar groove of the fibula where they are both within a common peroneal tendon sheath and stabilized by the superior peroneal retinaculum (<strong>Figure 10</strong>). From there, the peroneus longus tendon courses inferomedially along the plantar foot to insert on the lateral plantar aspect of the first metatarsal base and medial cuneiform, and the peroneus brevis courses anteriorly to insert on the lateral base of the fifth metatarsal.<sup>2</sup> The peroneus longus functions primarily in plantarflexion but also assists with eversion of the foot; the peroneus brevis functions primarily in eversion of the foot but also assists with ankle plantarflexion.<sup>12</sup></p>
<h3>Pathology</h3>
<p>Peroneal tendon pathology may result from acute injury or chronic repetitive trauma. Pathologic entities include tendinosis, tenosynovitis, tendon tears and injury to the superior peroneal retinaculum (SPR), which may predispose a patient to tendon subluxation or dislocation.<sup>3</sup></p>
<p>MR imaging has been described as the &ldquo;gold standard&rdquo; for imaging peroneal tendon pathology, and is a well-established technique to visualize fixed subluxation/dislocation of the peroneal tendons.<sup>3,6,13,14 </sup>Normally, peroneus longus is anterior and slightly lateral (or superficial) to the peroneus brevis, which is more posterior and medial, abutting the posterior cortex of the distal fibula. The supramalleolar tendons are relatively equal in size on axial MR and short-axis US (<strong>Figure 11</strong>). Normal peroneal tendons appear hypointense on MRI, as oval echogenic structures on short-axis US (<strong>Figure 12A</strong>), and demonstrate linear, fibrillar echotexture on long-axis US (<strong>Figure 12B</strong>).</p>
<p>Tenosynovitis is seen as T2-hyperintense material on MR or anechoic material on US contained within the tendon sheath, surrounding intact tendons (<strong>Figure 13</strong>). Tendinosis is seen as thickening of the intact tendons, with intermediate T2 signal intensity on MRI and hypoechogenicity and architectural distortion on US and can range from mild tendinosis (<strong>Figure 14</strong>) to severe tendinosis with early instrasubstance tearing (<strong>Figure 15</strong>). Longitudinal split tears, most commonly affecting the peroneus brevis tendon, are seen as an anechoic or hypoechoic linear defect paralleling the tendon fibers on long-axis imaging, or can be demonstrated by separating the tendon into two distinct components on short-axis imaging (<strong>Figure 16</strong>). The presence of three distinct tendons on short-axis US or axial MR images is diagnostic of a longitudinal split tear. Full thickness tears are much less common but may occur in tendons with longstanding or severe tendinosis. Occasionally, a full thickness tear of the peroneus longus tendon may be detected radiographically by noting proximal displacement of an os peroneum (<strong>Figure 17</strong>).</p>
<p>SPR tears and resultant peroneal tendon subluxation/dislocation are also well visualized by US. Peroneal tendon subluxation is most commonly found in athletes, resulting from disruption of the superior peroneal retinaculum (SPR), and is often associated with dorsiflexion of the ankle and concomitant eversion or inversion of the foot.<sup>3,14</sup> Although the retinaculum is not directly visualized radiographically, an avulsion fracture of the lateral, distal fibular cortex may be identified, indicating SPR deficiency (<strong>Figure 18</strong>). Peroneal tendon subluxation is relatively uncommon, occurring in 0.3% to 0.5% of traumatic ankle injuries, and is frequently masked by other ankle pathologies or misdiagnosed as an ankle sprain.<sup>2,3,15</sup> However, accurate diagnosis of pathologic peroneal tendon subluxation is critical, as conservative measures are often inadequate and surgery is commonly required for complete return of function and symptom resolution.</p>
<p>MRI and US may directly demonstrate disruption of the superior peroneal retinaculum and resultant fixed subluxation/dislocation of the peroneal tendons (<strong>Figure 19</strong>). Transient, or dynamic, tendon subluxation or dislocation is more difficult to assess on MR, but US is ideal for assessing dynamic peroneal tendon subluxation, as the tendons can be visualized in real time. During dynamic US evaluation, the patient performs provocation maneuvers such as ankle dorsiflexion and plantarflexion or circumduction, while the peroneal tendons are imaged in the short axis.<sup>15,16</sup> Displacement of the peroneal tendons lateral to the fibular cortex is diagnostic.</p>
<p>A specific subtype of peroneal subluxation is intrasheath subluxation, during which the peroneus longus and brevis tendons reverse their normal position in the common peroneal tendon sheath but remain within the retromalleolar groove, with an intact retinaculum.<sup>15</sup> (<strong>Figure 20</strong>) Patients with intrasheath subluxation may present with &ldquo;popping&rdquo; or &ldquo;snapping&rdquo; during ankle circumduction, as the tendons are displaced. It is unknown whether intrasheath peroneal tendon subluxation represents a pathologic entity or is a result of normal supramalleolar peroneal tendon motion. Therefore, it is important to note any symptom reproduction during the dynamic US examination.</p>
<h3>Anatomic Variants</h3>
<p>Aside from traumatic injuries, several anatomic variants of the lateral ankle may predispose a patient to peroneal tendon pathology. Lack of concavity of the distal posterior fibula of the retromalleolar groove may predispose a patient to peroneal tendon dislocation and subluxation.<sup>2,14,17</sup> Additionally, a prominent peroneal tubercle on the lateral calcaneus may predispose a patient to peroneal tendon pathology. Anatomic variations in muscles, such as a peroneus quartus muscle or a low-lying peroneus brevis muscle belly may cause crowding of the tendons in the retromalleolar groove, leading to pathology.<sup>2,3,13</sup></p>
<h2>Other Pathology of the Lateral Ankle</h2>
<p>Anterolateral ankle impingement is a distinct entity, often seen in young, athletic patients, and is likely secondary to repetitive microtrauma and microinstability.<sup>18</sup> Over time, microtrauma results in excessive hemorrhage, scar tissue formation and synovial hypertrophy in the lateral gutter of the ankle, eventually leading to impingement. The lateral gutter is defined by the tibia (posteromedially), fibula (laterally), tibiotalar joint capsule, ATFL and CFL (anterolaterally). As there is no associated high-grade ligamentous injury, these patients present with a stable ankle on examination, but often have decreased dorsiflexion and a palpable soft-tissue mass at the anterolateral ankle.</p>
<p>Another subgroup of patients with anterolateral ankle impingement includes those with an accessory ligament or thickened distal fascicle of the anteroinferior tibiofibular ligament, a normal variant that may be present in 21% to 97% of ankles.<sup>9,10,19 </sup>In these patients, a prior lateral ankle sprain results in ligamentous instability, which allows for anterior extrusion of the talar dome and increased pressure at the anterolateral ankle during dorsiflexion.<sup>9</sup> Over time, this leads to synovial hypertrophy and impingement of soft tissues between the anterolateral talus and the accessory anteroinferior tibiofibular ligament. Both MRI and US can identify synovial/capsular hypertrophy in the anterolateral gutter, seen as heterogenous synovial mass on US and T1/T2 intermediate- to low-signal synovial hypertrophy and scar tissue in the anterolateral gutter on MRI (<strong>Figure 21</strong>).</p>
<p>Extra-articular soft-tissue and osseous impingement may also occur at the lateral ankle. Talocalcaneal and subfibular impingement may occur in the setting of pes planovalgus secondary to lateral shift of weight-bearing forces from the talar dome to the lateral talus and fibula (<strong>Figure 22</strong>).<sup>20</sup> Eventually, progressive deformity leads to secondary osteoarthritis of the subtalar, talonavicular, and calcaneocuboid joints. MRI can provide detailed information about intra-articular pathology such as osteochondral lesions, osteoarthritis, and marrow edema-like signal in the setting of acute trauma and contusion.</p>
<p>Finally, articular-based processes such as synovial chondromatosis, pigmented villonodular synovitis, and inflammatory arthropathies, as well as crystalline deposition diseases such as gout and pseudogout, may be seen in the ankle. Although these often result in diffuse symptoms, they can present with lateral ankle pain if disease is asymmetric or focal.</p>
<h2>Conclusion</h2>
<p>Lateral ankle pain most commonly results from osseous, ligamentous or tendinous injury, but other etiologies should be considered in the nontraumatic setting. Although radiographs are an important first line of imaging, MRI and US can provide important diagnostic information regarding soft-tissue pathology around the ankle and should be considered in patients with lateral ankle pain.</p>
<h2>References</h2>
<ol>
<li>Kerkhoffs GM, Van Dijk CNV. Acute lateral ankle ligament ruptures in the athlete. Foot Ankle Clin 2013;18(2):215-218.</li>
<li>Niemi WJ, Savidakis J Jr., DeJesus JM. Peroneal subluxation: a comprehensive review of the literature with case presentations. J Foot Ankle Surg 1997;36.2:141-145.</li>
<li>Saragas NP, Ferrao PNF, Mayet Z, Eshraghi H. Peroneal tendon dislocation/subluxation &ndash; case series and review of the literature. Foot Ankle Surg 2016;22(2)125-130.</li>
<li>Brockett CL, Chapman GJ. Biomechanics of the ankle. Orthop Trauma 2016;30(3):232-238.</li>
<li>Kijowski R Blankenbaker DG, Shinki K, Fine JP, Graf BK, De Smet AA. Juvenile versus adult osteochondritis dissecans of the knee: appropriate MR imaging criteria for instability. Radiology 2008;248(2):571-578.</li>
<li>Rosenberg ZS, Beltran J, Bencardino JT. MR imaging of the ankle and foot. RadioGraphics 2000;20(suppl_1).</li>
<li>Golan&oacute; P, Vega J, Leeuw PA, et al. Anatomy of the ankle ligaments: a pictorial essay. Knee Surg, Sports Traumatol, Arthrosc 2010;18(5):557-569.</li>
<li>Hermans JJ, Beumer A, Jong TAWD, Kleinrensink G-J. Anatomy of the distal tibiofibular syndesmosis in adults: a pictorial essay with a multimodality approach. J Anat 2010;217(6):633-645.</li>
<li>Bassett FH 3rd, Gates HS 3rd, Billys JB, Morris HB, Nikolaou PK. Talar impingement by the anteroinferior tibiofibular ligament: a cause of chronic pain in the ankle after inversion sprain. J Bone Joint Surg Am 1990;72:55-59.</li>
<li>Subhas N, Vinson EN, Cothran RL, Santangelo JR, Nunley JA 2nd, Helms CA. MRI appearance of surgically proven abnormal accessory anterior-inferior tibiofibular ligament (Bassett&rsquo;s ligament). Skeletal Radiol 2008;37:27-33.</li>
<li>Hoefnagels EM, Waites MD, Wing ID, Belkoff SM, Swierstra BA. Biomechanical comparison of the interosseous tibiofibular ligament and the anterior tibiofibular ligament. Foot Ankle Int 2007;28:602-604.</li>
<li>Davda K, Malhotra K, O&rsquo;Donnell P, Singh D, Cullen N. Peroneal tendon disorders. EFORT Open Reviews 2017;2(6):281-292.</li>
<li>Mirmiran R, Squire C, Wassell D. Prevalence and role of a low-lying peroneus brevis muscle belly in patients with peroneal tendon pathologic features: a potential source of tendon subluxation. J Foot Ankle Surg 2015;54:872-875.</li>
<li>Mendicino RW, Orsini RC, Whitman SE, Catanzariti AR. Fibular groove deepening for recurrent peroneal subluxation. J Foot Ankle Surg 2001;40(4)252-263.</li>
<li>Neustadter J, Raikin SM, Nazarian LN. Dynamic sonographic evaluation of peroneal tendon subluxation. Am J Roentgenol 2004;183(4):985-988.</li>
<li>Pesquer L, Guillo S, Poussange N, Pele E, Meyer P, Dallaudiere B. Dynamic ultrasound of peroneal tendon instability. Br J Radiol 2016;89:20150958.</li>
<li>Van Dijk PAD, Vopat BG, Guss D, Younger A, DiGiovanni CW. Retromalleolar groove deepening in recurrent peroneal tendon dislocation: technique tip. Orthop J Sports Med 2017;5(5):2325967117706673.</li>
<li>Kim SH, Ha KI. Arthroscopic treatment for impingement of the anterolateral soft tissues of the ankle. J Bone Joint Surg Br 2000;82:1019-1021.</li>
<li>Donovan A, Rosenberg ZS. MRI of ankle and lateral hindfoot impingement syndromes. Am J Roentgenol 2010;195(3):595-604.</li>
<li>Friedman MA, Draganich LF, Toolan B, Brage ME. The effects of adult acquired flatfoot deformity on tibiotalar joint contact characteristics. Foot Ankle Int 2001;22:241-246.</li>
</ol>9846Evaluation of Common Pathology of the Elbow Utilizing Dynamic Ultrasound and MRI2020-01-24T11:16:16-05:002020-01-24T11:16:16-05:00Kelli Rosen, D.O., Leah Davis, D.O., Courtney Scher, D.O.<p>Musculoskeletal ultrasound (US) is an ideal imaging modality for assessing elbow joint anatomy and pathology. The elbow joint is particularly amenable to US evaluation as it is a small joint with 360-degree accessibility by the transducer and is easily manipulated, both actively by the patient and passively by the examiner.<sup>1</sup> Beyond diagnostics, US can also aid in image-guided treatment of certain conditions.</p>
<p>MRI also plays an important role in evaluating the elbow. In addition to soft-tissue anatomy and pathology, MRI also depicts radiographically occult fractures, bone contusions, and intra-articular pathology exquisitely.<sup>2</sup> Magnetic resonance arthrography (MRA) utilizing gadolinium-based contrast placed directly into the joint allows for optimal evaluation of articular cartilage/intracapsular structures, intra- articular loose bodies, and the collateral ligaments.<sup>1,2</sup></p>
<p>This article will review the anatomy and pathology of the elbow joint and review the US examination by compartment, featuring the most pertinent anatomic structures and their related pathology (<strong>Table 1</strong>). Correlative MRI evaluation of the elbow joint and pathology will also be discussed.</p>
<h2>Osseous Articulations</h2>
<p>The ulnohumeral articulation is a hinge joint, providing the majority of flexion and extension motion at the elbow. The radiocapitellar articulation is a &ldquo;hinge and pivot&rdquo; joint without inherent osseous mobility. The proximal radioulnar joint, held in place by the annular ligament, allows for rotation of the radial head in the sigmoid notch of the ulna in supination and pronation. These three articulations, as well as anterior and posterior fat pads, are encased by the joint capsule.<sup>3</sup></p>
<p>Many muscles, tendons, ligaments, and nerves work together with this bony foundation to create the elegant, dynamic, and complex function of the elbow joint. These structures and their related pathologies will be discussed further, based on the compartment in which they reside.</p>
<h2>Anterior Compartment</h2>
<p>Structures of interest in the anterior elbow include the joint recess, distal biceps tendon insertion, brachialis muscle, as well as the median and radial nerves (<strong>Figure 1</strong>).<sup>4,5 </sup></p>
<p>The biceps brachii, composed of a long head originating from the supraglenoid tubercle and a short head from the coracoid process, crosses the shoulder and elbow joints. As it courses distally over the anterior humerus, the muscle bellies of the lateral long head and medial short head gradually, but incompletely, insinuate with one another. Just proximal to the elbow joint, the biceps brachii muscle separates again into two distinct tendon heads. Both heads contribute to the distal biceps tendon coursing through the cubital fossa and inserting on the radial tuberosity.<sup>6</sup></p>
<p>Evaluation of the distal biceps tendon (DBT) can be challenging due to its oblique course and deep insertion.<sup>4,5 </sup>The normal tendon may appear hypoechoic as it dives deep, secondary to an artifact known as anisotropy.<sup>1</sup> Keeping the probe parallel to the tendon in long axis and perpendicular in short axis is important for avoiding this artifact and causing subsequent misinterpretation. Long-axis images are ideal for evaluating the distal biceps tendon insertion on the radial tuberosity (<strong>Figure 2</strong>).<sup>4,5 </sup></p>
<p>At the anterolateral aspect of the elbow, the radial nerve and its posterior interosseous branch (PIN) can be visualized. Of note, it is important to visualize the PIN as it pierces and then travels through the two heads of the supinator muscle and the Arcade of Frohse (<strong>Figure 3</strong>). The course of the PIN, as it travels from the anterior to the posterior compartments, may be obtained in the transverse plane as the subject pronates the forearm.<sup>4,5 </sup></p>
<h3>Distal Biceps Tendon Tear</h3>
<p>The biceps tendon is the most powerful forearm supinator and is the most commonly torn tendon in the elbow. Injury is common at or near the insertion of the DBT on the radial tuberosity, owing to its relative hypovascularity in this location.<sup>1</sup> Tendon rupture most often results from acute trauma rather than overuse, and is relatively common in rugby players and weight lifters when the arm is forcefully extended against a flexed elbow.<sup>7</sup> Of note, rupture of the proximal long-head biceps tendon at the shoulder joint is approximately 10 times more common than rupture of the DBT at the elbow.<sup>7</sup></p>
<p>In the setting of complete tendon rupture, the lacertus fibrosus may prevent retraction of the DBT proximally. If the lacertus fibrosus is also torn, a complete tear can present as a palpable painful mass over the proximal anterior arm. Early diagnosis of a complete DBT tear is critical, as clinical outcome is greatly improved with early surgical intervention within the first few weeks following injury. This is in contrast with tears of the proximal biceps tendon, where conservative treatment is the therapy mainstay.<sup>7</sup></p>
<p>Complete tear of the DBT is amenable to US diagnosis. Findings include nonvisualization of the tendon at the insertion site with hypoechoic fluid collection/hematoma in the tendinous bed (<strong>Figure 4</strong>). Partial tears of the DBT are often more difficult to diagnose by US compared to MRI. In the setting of partial DBT tear, the thinned tendon will assume an irregular, attenuated profile or wavy contour (<strong>Figure 5</strong>).<sup>7</sup></p>
<p>MRI is particularly useful for diagnosing a DBT injury and discerning the degree of severity. DBT is best evaluated on axial images, although fluid-sensitive sagittal images can help confirm a complete rupture and estimate the degree of stump retraction. Focal T2 hyperintensity in and adjacent to the DBT indicate a partial tear (<strong>Figure 5</strong>).<sup>7</sup></p>
<h2>Lateral Compartment</h2>
<p>Important lateral elbow structures to evaluate include the common extensor tendon, lateral collateral ligament complex, and radiocapitellar joint.<sup>4,5</sup></p>
<p>Placement of the transducer longitudinally over the lateral epicondyle will reveal the radiocapitellar articulation, radial collateral ligament (RCL), and overlying thin, long common extensor tendon (CET) (<strong>Figure 6</strong>).<sup>1</sup></p>
<p>The CET is best visualized on the coronal plane/long axis and is composed of the origins of the extensor carpi radialis longus and brevis, extensor digiti minimi, and extensor digitorum communis tendons.<sup>4,5</sup> On US, the CET is a smooth hyperechoic beak-shaped structure originating from the anterolateral aspect of the lateral epicondyle, with the radial collateral ligament just deep to the tendon origin (<strong>Figure 6</strong>).<sup>1 </sup>The radiocapitellar joint is visible deep to the CET and the ligament.<sup>4,5</sup></p>
<h3>Lateral Epicondylitis</h3>
<p>Lateral epicondylitis is the most common sports-related elbow injury, classically seen in tennis players, but is also commonly seen secondary to repetitive work-related activities.<sup>7</sup></p>
<p>Lateral epicondylitis involves the common extensor tendon origin at the lateral epicondyle, with the extensor carpi radialis brevis tendon the most commonly affected.<sup>8</sup> Despite the &ldquo;-itis&rdquo; suffix, lateral epicondylitis is degenerative in nature, resulting from overuse of the extensor and supinator muscles.<sup>7,8</sup></p>
<p>Tendinosis can be recognized by US as an abnormal hypoechoic thickened appearance of the CET origin. Areas of osseous irregularity underlying the CET may be present with hyperemia seen during color or power Doppler interrogation (<strong>Figure 7</strong>). An anechoic cleft with complete or incomplete disruption of tendon fibers will be seen with partial and full thickness tears, respectively.</p>
<p>On MRI, lateral epicondylitis is demonstrated by intermediate T1- and increased T2-weighted signal representative of intratendinous mucoid degeneration and neovascularization (<strong>Figure 7</strong>). These findings result from microscopic tearing and formation of reparative tissue. Over time, macroscopic tearing or injury to the radial collateral ligamentous complex may also occur. Many secondary findings suggestive of lateral epicondylitis may be observed: bone marrow edema, periostitis of lateral epicondyle, anconeous muscle edema, or fluid in the radial head bursa.<sup>7</sup></p>
<p>Of special importance in the setting of lateral elbow trauma, is evaluation for concomitant injury of the CET and underlying lateral collateral ligament complex, which can result in posterolateral rotary instability (PLRI). Tears of the RCL are especially important to note as surgical debridement of the CET could result in further destabilization of an already injured RCL.<sup>7</sup></p>
<p>The lateral ulnar collateral ligament (LUCL) is a component of the lateral collateral ligament complex. It arises from the inferior surface of the lateral epicondyle, taking an oblique medial course to insert on the proximal ulna. It is a primary restraint to varus stress of the elbow and when injured, can also contribute to PLRI. The LUCL is best visualized on coronal MRI sequences (<strong>Figure 8</strong>).<sup>9</sup> It is not reliably well visualized by US.</p>
<h2>Medial Compartment</h2>
<p>US evaluation of the medial elbow is primarily performed to evaluate the common flexor tendon (CFT), ulnar collateral ligament (UCL), and the ulnar nerve.<sup>4,5 </sup></p>
<p>The CFT origin on the medial epicondyle of the humerus includes the flexor carpi radialis and ulnaris, palmaris longus, flexor digitorum superficialis, and pronator teres tendons. Positioning the transducer longitudinally with the proximal aspect over the medial epicondyle will reveal the CFT in long axis (<strong>Figure 9</strong>).<sup>1</sup></p>
<p>The UCL is the primary static stabilizer of the elbow against valgus stress.<sup>1</sup> With the probe oriented obliquely longitudinally over the medial epicondyle, the anterior bundle of the UCL will be visible in long axis (<strong>Figure 10</strong>). Dynamic imaging of the UCL with valgus stress on the ulnohumeral joint should also be performed for complete assessment. Subsequent joint space widening will accentuate ligament laxity, if present, and may reveal a partial tear of the ligament.<sup>4,5</sup></p>
<p>At the level of the cubital tunnel, the ulnar nerve can be well evaluated. In cross-section/short axis, the nerve will appear as a hypoechoic rounded structure surrounded by echogenic fat, creating a honeycomb appearance (<strong>Figure 11</strong>).<sup>1</sup></p>
<p>Dynamic maneuvers can be performed while visualizing the ulnar nerve in short axis to assess for subluxation or dislocation over the medial epicondyle during elbow flexion.<sup>4,5</sup></p>
<h3>Medial Epicondylitis</h3>
<p>Medial epicondylitis, also known as golfer&rsquo;s or pitcher&rsquo;s elbow, develops in the setting of overuse or trauma and involves the CFT at its origin, most commonly affecting the pronator teres and flexor carpi radialis tendons.<sup>4,5,8</sup> Patients may complain of aching pain over the medial elbow and, in chronic cases, grip strength may weaken.<sup>7</sup> Medial epicondylitis is much less common than lateral epicondylitis.<sup>7</sup></p>
<p>US is an important modality for diagnosing medial epicondylitis and is especially useful to distinguish medial epicondylitis from a tear of the deeper UCL.<sup>7</sup> Tendinosis can be recognized as abnormally thick, hypoechoic areas in the CFT at its origin (<strong>Figure 12</strong>). Additionally, areas of bony irregularity of the medial epicondyle may be present, as well as peritendinous fluid, hyperemia, or soft-tissue swelling.<sup>7,8 </sup>An anechoic cleft with complete or incomplete disruption of tendon fibers will be seen with partial and full thickness tears, respectively.<sup>8</sup> Because of the close spatial and functional relationship of the CFT, UCL, and ulnar nerve, these structures are susceptible to concomitant injury. As many as 60% of patients undergoing surgery for medial epicondylitis have been found to exhibit signs of ulnar nerve neurapraxia.<sup>7,10</sup></p>
<p>MRI imaging in the setting of medial epicondylitis demonstrates increased T1- and T2-weighted signal, representative of intratendinous mucoid degeneration and neovascularization as a result of microscopic tearing and formation of reparative tissue. Over time, macroscopic tearing may occur.<sup>7</sup></p>
<h3>Injury to the Anterior Band of the Ulnar Collateral Ligament</h3>
<p>The most clinically relevant and commonly injured component of the UCL is the anterior band that extends from the undersurface of the medial epicondyle to the sublime tubercle on the proximal ulna.<sup>4,5</sup> The UCL is a primary elbow joint stabilizer, providing nearly 50% of the protection against valgus stress. Injury to the anterior band of the UCL is classically seen in overhead throwing athletes, especially pitchers, secondary to repetitive microtrauma in the form of valgus stress (<strong>Figure 13</strong>). Acute trauma, such as a fall on an outstretched arm, or posterior elbow dislocation, is a less common cause of UCL injury.<sup>7</sup></p>
<p>On MRI, the UCL is normally homogeneous and hypointense on all sequences. Injury to the UCL is best displayed on coronal MRI images, where it will appear as T2 hyperintense, discontinuous, and ill-defined in shape. While increased signal alone may not be indicative of a tear, signal abnormality with architectural distortion is.<sup>11</sup> Acute injury is also suggested by flexor digitorum superficialis muscle and/or periligamentous edema (<strong>Figure 13</strong>).<sup>7 </sup></p>
<p>Partial tear or sprain of the UCL presents as hypoechoic thickening and/or heterogeneity of the ligament without complete fiber disruption (<strong>Figure 14</strong>). Ligament laxity, demonstrated with valgus stress maneuvers, without ligamentous disruption may indicate remote injury, partial tear, or acquired laxity in high-level overhead athletes such as baseball pitchers. Complete fiber disruption signifies a full thickness tear. In the acute setting with hemorrhage and edema, it may be difficult to discern full and partial thickness tears. Again, dynamic imaging with valgus stress may reveal separation of torn ligament ends, suggesting complete tear.</p>
<p>Of note, professional or high-level amateur pitchers may demonstrate areas of hypoechogenicity or foci of calcification, ligamentous thickening, and laxity without symptoms, especially during the sporting season (<strong>Figure 15</strong>).<sup>8</sup></p>
<h3>Ulnar Nerve Injury</h3>
<p>The ulnar nerve at the medial elbow is prone to injury or entrapment, especially as it passes beneath the cubital tunnel and the retinaculum between the medial epicondyle of the humerus and olecranon process. Etiologies for ulnar nerve injury at the elbow include acute trauma, overuse or repetitive injury, and nerve subluxation or dislocation.<sup>8</sup></p>
<p>Ulnar nerve entrapment, or cubital tunnel syndrome, is a common elbow pathology. US will reveal an enlarged, hypoechoic ulnar nerve proximal to the cubital tunnel (<strong>Figure 16</strong>). Within the tunnel, the nerve often normalizes in size. A maximal cross-sectional diameter of the ulnar nerve &gt; 9 mm sq, or a change in caliber &gt; 2-3 mm sq proximal to or within the cubital tunnel, suggests pathology.<sup>8</sup></p>
<p>Dynamic evaluation may reveal the ulnar nerve dislocating over the medial epicondyle during elbow flexion, with relocation in extension. While this transient dislocation may be seen with ulnar nerve irritation/injury or injury to the overlying Osborn&rsquo;s ligament, up to 20% of the asymptomatic population will demonstrate this variation.<sup>8</sup></p>
<p>In contrast, dynamic imaging may also demonstrate dislocation of the medial head of the triceps tendon and the ulnar nerve over the cubital tunnel and medial epicondyle with flexion. This phenomenon is referred to as snapping triceps syndrome and is considered a pathologic entity.<sup>7</sup></p>
<p>MRI can also be used to evaluate the ulnar nerve as it courses through the cubital tunnel.<sup>1</sup> The benefit of US assessment includes superior resolution and magnification of the nerve, as well as the ability to perform a dynamic examination.</p>
<h2>Posterior Compartment</h2>
<p>Structures of importance in the posterior elbow include the triceps tendon, olecranon bursa and the posterior joint recess.<sup>4,5</sup> The triceps tendon appears as a short, broad, echogenic fibrillar structure inserting on the olecranon (<strong>Figure 17</strong>).<sup>1</sup></p>
<p>Pay close attention to probe pressure over the superficial olecranon bursa, as increased pressure may shift small bursal effusions out of view.<sup>4,5</sup></p>
<h3>Triceps Tendon Injury</h3>
<p>Injury to the triceps tendon or muscle is relatively uncommon and may be post-traumatic, spontaneous, or degenerative. When it is sports related, weight lifters, bowlers, baseball pitchers, and football players are most often affected with post-traumatic injuries.<sup>7,8</sup> Spontaneous injury to the triceps tendon can be seen in patients with systemic illnesses, such as lupus, chronic renal failure with secondary hyperparathyroidism, rheumatoid arthritis, and other conditions for which steroid therapy is utilized.<sup>4,5</sup></p>
<p>Tears of the distal triceps tendon (DTT) may be full or partial thickness and often involve the combined lateral and long heads. Most tears are incomplete with the short muscular medial head attachment remaining intact.<sup>8</sup> Complete tendon disruption and a variable degree of tendon retraction can be seen following a full-thickness tear, with the tendon itself appearing lax and heterogenous (<strong>Figure 18</strong>). In the setting of radial head fracture, be careful to evaluate for DTT injury, as they occur with similar injury mechanisms.<sup>7,8 </sup></p>
<h3>Olecranon Bursitis and Joint Pathology</h3>
<p>Rheumatoid arthritis, gout, infection, and hemorrhage, whether spontaneous or post-traumatic, are potential etiologies of bursal or joint distention with complex-appearing fluid. In patients with gout, evaluation may reveal hyperechoic synovial hypertrophy with internal hyperechoic foci/crystals (<strong>Figure 19</strong>). Synovial hypertrophy will demonstrate increased color or power Doppler flow, while lack of internal flow on color Doppler suggests complex fluid (<strong>Figure 20</strong>).<sup>8</sup></p>
<h2>Injection and Aspiration</h2>
<p>In addition to its diagnostic capabilities, US is an ideal modality for image-guided intervention in and around the elbow joint. In the setting of osteoarthritis, inflammatory or crystalline arthropathy, US can guide joint aspiration and steroid injection. When an infectious etiology is suspected, US-guided joint aspiration can confirm diagnosis, allowing for timely treatment.</p>
<p>Dry needling, or repeated lancing of an abnormal area of tendon to incite internal hemorrhage and elicit the consequent inflammatory response, is felt to promote healing and granulation tissue formation. Peritendinous steroid injection may also be performed with US guidance, taking care to not inject steroids into the tendon itself; intratendinous steroid injection increases the likelihood of post-procedure tendon rupture and should be avoided.<sup>12</sup></p>
<p>The olecranon bursa is also amenable to injection and/or aspiration when distended with fluid or thickened synovial tissue. Steroid injection should not be performed if septic bursitis is suspected.<sup>12 </sup></p>
<h2>Conclusion</h2>
<p>In summary, US is a useful tool in the diagnostic evaluation and treatment of the elbow joint and related pathologies. US is particularly beneficial in evaluating the superficial structures of the elbow including the tendons, muscles and ligaments. The dynamic capabilities of US allow for additional evaluation of the structural integrity of the ulnar collateral ligament, ulnar nerve and triceps tendon. During image-guided intervention, US allows for patient comfort adaptations in addition to providing exceptional anatomic visualization.</p>
<p>MRI examination of the elbow allows for exquisite visualization of the deeper intra-articular structures including the cartilage and bone marrow, as well as the tendons, muscles, and ligaments. However, a benefit of US includes its ability to obtain dynamic imaging of the joint. These principles should be considered when choosing the optimal imaging modality for diagnostic purposes, as well as intervention of the elbow and related pathologies.</p>
<h2>References</h2>
<ol>
<li>Pope T, Beltran J, Bloem HL, et al. 10. In: Musculoskeletal Imaging. 1st Ed. Philadelphia, PA: Elsevier Health Sciences, 2015:134-147.</li>
<li>Pope T, Beltran J, Bloem HL, et al. 10. In: Musculoskeletal Imaging. 1st ed. Philadelphia, PA: Elsevier Health Sciences, 2015:148-156.</li>
<li>Manaster BJ, Miller TT. Elbow Overview. RADPrimer. https://app.radprimer.com/document/d724eeff-a489-4f47-a8e5-9271da9e9b90/lesson/7a444fbb-2bdb-4c84-ac85-a47f80132470. Accessed March 2019.</li>
<li>Beggs I, Bianchi S, Bueno A. Elbow. In: Musculoskeletal Ultrasound Technical Guidelines. Vienna, Austria: European Society of MusculoSkeletal Radiology.</li>
<li>Martinoli C. Musculoskeletal ultrasound: technical guidelines. Insights Imag 2010;1(3):99-141.</li>
<li>Dirim B, Brouha SS, Pretterklieber ML, et al. Terminal bifurcation of the biceps brachii muscle and tendon: anatomic considerations and clinical implications. Am J Roentgenol 2008;191(6):W248-255.</li>
<li>Pope T, Beltran J, Bloem HL, et al. In: Musculoskeletal Imaging. 2nd ed. Philadelphia, PA: Elsevier Health Sciences, 2015:157-168.</li>
<li>Jacobson JA. Fundamentals of Musculoskeletal Ultrasound. 3<sup>rd</sup> Ed. Philadelphia, PA: Elsevier; 2018;127-167.</li>
<li>Karbach LE, Elfar J. Elbow Instability: Anatomy, Biomechanics, Diagnostic Maneuvers, and Testing. J Hand Surg Am 2017;42(2): 118-126.</li>
<li>Maffulli N, Regine R, Carrillo F, Capasso G, Minelli S. Tennis elbow: an ultrasonographic study in tennis players. Br J Sports Med 1990;24(3): 151-154.</li>
<li>Husarik DB, Saupe N. Pfirrmann CW, Jost B, Hodler J, Zanetti M. Ligaments and plicae of the elbow: normal MR imaging variability in 60 asymptomatic subjects. Radiology 2010;257(1): 185-194.</li>
<li>Allen GM, Wilson DJ. Ultrasound guided musculoskeletal injections. Philadelphia, PA: Elsevier, 2018;85-112.</li>
</ol>9824TB or Not TB: Differential Diagnosis and Imaging Findings of Pulmonary Cavities2019-09-27T10:01:53-04:002019-09-27T10:01:53-04:00Yoon Cho, D.O., Jeff Lee, D.O., Christos Vassiliou, D.O., Donald von Borstel, D.O.<p>Cavitary lesions are often encountered during radiographic evaluation of the chest. During early radiology training, residents are introduced to the mnemonic &ldquo;CAVITY&rdquo; for the differential diagnosis of pulmonary cavitary lesions: cancer (bronchogenic carcinoma, especially squamous cell carcinoma), autoimmune (granulomatosis with polyangiitis or rheumatoid arthritis), vascular (pulmonary emboli &ndash; septic or bland), infection (tuberculosis, fungal, <em>staphylococcus aureus</em>), trauma (pneumatocele or laceration), and youth (congenital pulmonary airway malformation, pulmonary sequestration, bronchogenic cyst).<sup>1</sup> Although this mnemonic is an efficient way of expanding the differential diagnosis for novice radiologists, a deeper understanding of each condition is necessary to make the correct diagnosis in practice. In addition, these differentials must be given in the appropriate clinical context. This article will discuss imaging findings of common cavitary lesions, which along with clinical history, can lead to the correct diagnosis and expedite appropriate management.</p>
<h2>Cavity or Pulmonary Cyst</h2>
<p>To arrive at the correct diagnosis, the difference between pulmonary cysts and cavities must be defined. According to the Fleischner Society, a pulmonary cyst is &ldquo;any round circumscribed space surrounded by an epithelial or fibrous wall.&rdquo; The wall thickness of the cyst is usually &lt; 2 mm.<sup>2</sup></p>
<p>Meanwhile, a pulmonary cavity is defined as &ldquo;a gas-filled space that is seen as a lucency or low-attenuation area within a pulmonary consolidation, mass, or a nodule&rdquo; (<strong>Figure 1</strong>).<sup>2</sup> Wall thickness of a cavitary lesion is usually &gt; 2 to 4 mm. Wall thickness also helps to predict malignancy of a lesion. Cysts or cavities with wall thickness &lt; 4 mm are likely benign, while wall thickness &gt; 15 mm suggests malignancy.<sup>3</sup></p>
<p><strong>Table 1</strong> includes a broad differential diagnosis of both pulmonary cysts and cavities.</p>
<h2>Bleb/Bulla</h2>
<p>Blebs and bullae are often incidentally found in asymptomatic patients, mostly in thin younger males or patients with an extensive smoking history. Blebs are formed as a result of spontaneous rupture of subpleural alveoli. Both are usually located in the periphery of lungs with thin walls &lt; 1 mm. The main distinction between blebs and bullae is size (<strong>Figure 2</strong>). Blebs are defined as a &ldquo;small gas-containing space within the visceral pleura or in the subpleural lung, not larger than 1 cm in diameter.&rdquo;<sup>2</sup> Bullae are defined as &ldquo;airspace measuring &gt; 1 cm in diameter, sharply demarcated by a thin wall that is no greater than 1 mm in thickness.&rdquo;<sup>2</sup> Reporting large bullae is important as they can rupture, resulting in a pneumothorax.</p>
<h2>Cancer</h2>
<h3>Bronchogenic Carcinoma</h3>
<p>There are 3 proposed mechanisms of how primary lung cancer presents as a cystic mass. The first mechanism is by having a rapid growth of lung cancer during which the blood supply cannot meet the demand of the neoplastic growth and causes central necrosis of the tumor.<sup>3</sup> The second mechanism is due to mass effect causing bronchial obstruction, scarring, or bronchiectasis resulting in infection distal to the obstructive mass; infection later leads to the breakdown of the lung parenchyma and forms the cystic cavity. The third mechanism is by &ldquo;spillover abscess,&rdquo; which describes spillage of the primary infection to the distant site of cavitation, even involving different lobes of the lung.<sup>4</sup></p>
<p>Cavitating lung cancer is most often seen in the sixth to seventh decades of life in patients with significant smoking history. Unfortunately, cavitation in primary lung cancer is associated with a poor prognosis. Out of all the types of primary lung carcinoma, squamous cell carcinoma is most commonly associated with cavitary lesions.<sup>4</sup> Cavitary lesions are rarely associated with small cell carcinoma. Findings associated with primary lung cancer include thick and irregular inner walls. Cavity size varies from 1 to 10 cm. According to a study by Woodring et al, most cavitary lesions with wall thickness &lt; 4 mm were benign, &gt;15 mm were malignant, and between 4 and 15 mm had mixed results.<sup>3,5</sup></p>
<h3>Metastasis</h3>
<p>Cavitation of lung metastases from extrapulmonary primary cancer is uncommon, occurring in only 4% of cases.<sup>5 </sup>The average age for presentation with pulmonary metastasis is 60 to 70 years. The most common primary origin of pulmonary metastatic disease is squamous cell cancer of the head and neck. Other primary sites include large intestine, cervix, stomach, esophagus, pancreas, and kidney. Cavitation size varies from 1 to 6 cm, and the wall thickness also varies from 0.3 to 2.5 cm.<sup>5</sup> Similar to primary lung cancer, thick and irregular walls are the most common imaging findings, and metastasis often presents with multiple cavities, mostly seen in the periphery of lungs (<strong>Figures 3 and 4</strong>). The diagnosis is often made by biopsy of the lesions due to their indeterminate imaging characteristics.</p>
<h2>Autoimmune (Cyst)</h2>
<h3>Lymphangioleiomyomatosis</h3>
<p>Lymphangioleiomyomatosis (LAM) is defined as progressive growth of smooth muscle cells in the pulmonary parenchyma, vasculature, lymphatics, and pleurae. LAM exclusively affects females 20 to 40 years old. The etiology of LAM is not well defined, but the close relationship between tuberous sclerosis and LAM suggests that somatic mosaicism on the TSC-2 gene may have a role.<sup>6</sup> Another theory is that LAM is associated with a metastatic neoplasm originating from the uterus, hence the reason for involving only the female population.<sup>7</sup> Most patients present with cough, hemoptysis, and chest pain. The symptoms may be exacerbated during pregnancy as estrogen level increases. Diagnosis can be made with CT, which demonstrates diffuse bilateral thin-walled cysts, measuring up to 5 mm in diameter, with associated hemorrhagic ground-glass opacities (<strong>Figure 5A</strong>).<sup>8</sup> When CT is not diagnostic, histopathologic diagnosis of smooth muscle cells can confirm the diagnosis. Other imaging manifestations of tuberous sclerosis include renal angiomyolipomas (<strong>Figure 5B</strong>) and cardiac rhabdomyomas.<sup>9</sup> LAM carries a poor prognosis as it can lead to progressive respiratory failure. Current treatment includes mTOR inhibitor (eg, Sirolimus) or lung transplant.<sup>6</sup></p>
<h3>Interstitial Lung Disease</h3>
<p>Interstitial lung disease (ILD) is a broad category encompassing many different idiopathic interstitial pneumonias. ILD affects the interstitium that surrounds alveoli. The most common and concerning condition with a poor prognosis is idiopathic pulmonary fibrosis (IPF). IPF most often occurs between ages 40 and 70 years. However, in patients who have more than 2 first-degree relatives with pulmonary fibrosis, this may present before their fifth decade.<sup>10</sup> As with all other types of interstitial pneumonia, IPF assessment is best performed with thin-section high-resolution CT (HRCT). Imaging findings of IPF are a definite or probable UIP pattern including general parenchymal volume loss, basilar and subpleural predominant fibrotic change, reticular abnormality, and honeycombing with or without traction bronchiectasis (<strong>Figure 6</strong>). The most defining characteristic of UIP/IPF on HRCT is the honeycombing fibrotic appearance, described as multilayered cystic changes ranging from 2 to 10 mm most commonly distributed in the lung bases. With the recent introduction of Pirfenidone treatment in these patients, the survival time among IPF patients improved by 52 weeks, from 2 to 3 years.<sup>11</sup> Five-year survival rate of IPF ranges from 30% to 50%. Pirfenidone and Nintedanib can be used in cases of mild to moderate disease to delay lung transplantation.<sup>10</sup></p>
<h3>Progressive Systemic Sclerosis (Scleroderma)</h3>
<p>Systemic sclerosis (SSc) is a connective tissue disorder characterized by progressive fibrosis of multiple organs, including the lungs, skin, vessels, and visceral organs. This condition is seen 4 times more often in women and commonly between ages 20 and 50. Patients with pulmonary involvement present with a restrictive lung disease pattern of low lung volumes, preserved flow rate, and low diffusion capacity. Interstitial lung disease can also develop, which is seen in about two-thirds of patients. On HRCT, either usual interstitial pneumonia (UIP) or nonspecific interstitial pneumonia (NSIP) pattern may be observed with variable presentation from early ground-glass opacities to late fibrosis.<sup>12</sup> Lung bases and subpleural spaces are most commonly affected. In some cases, cystic changes may occur with each cyst ranging from 1 to 5 cm in diameter (<strong>Figure 7</strong>). Dilation of the esophagus is a crucial finding and unique to SSc.<sup>13</sup> Once the lung disease has progressed to fibrosis/UIP, chances of disease reversal are poor. As of now, cyclophosphamide, glucocorticoids, or N-acetylcysteine can be attempted to halt disease progression. However, the efficacy of these treatments is better in earlier phases of the disease.<sup>12</sup></p>
<h3>Pulmonary Langerhans Cell Histiocytosis</h3>
<p>Langerhans cell histiocytosis (LCH) is a rare pediatric disease with male predilection that is mainly diagnosed between the ages of 1 and 3. As the name implies, LCH is caused by uncontrolled monoclonal proliferation of langerhan dendritic cells of the skin and other tissues contacting the external surface. The overactivation of the &ldquo;langerhans-like&rdquo; histiocytes begin to release large amount of oxidants, proteases, and fibronectin causing destruction of the lung parenchyma.<sup>14</sup> In addition to the wide-spread disseminated form, a pulmonary manifestation of this disease, also known as pulmonary langerhans cell histiocytosis, can be seen in young males between 20 to 40-years-old and is highly associated with smoking. The most common presenting symptoms are dyspnea and dry cough. Patients can also present with pleuritic chest pain, weight loss, or spontaneous pneumothorax. Classic imaging findings are thin-walled, small, irregular shaped cysts (usually less than 10mm in diameter) which are upper lobe predominant and associated small nodules.<sup>15</sup> Fibrotic changes can be observed in the later stages of disease. Prognosis is good with 50% of patients showing spontaneous resolution after smoking cessation. Corticosteroids are often used as a treatment option with good results.</p>
<h2>Autoimmune (Cavitary)</h2>
<h3>Granulomatosis with Polyangiitis</h3>
<p>Granulomatosis with Polyangiitis (GPA) is a multisystem necrotizing granulomatous vasculitis that affects primarily the small to medium-sized vessels and was previously termed &ldquo;Wegener granulomatosis.&rdquo;<sup>16</sup> The lungs are most commonly involved in this disease and the patients present with cough, hemoptysis, and dyspnea from ages 40 to 60.</p>
<p>Common imaging findings of the lungs include multiple, bilateral pulmonary masses with cavitation in more than 50% of the lesions. Cavitations are more common in the larger lesions and are thick with irregular, &ldquo;shaggy&rdquo; cavity walls (<strong>Figure 8</strong>).<sup>17</sup> This pulmonary disease can also present with alveolar hemorrhage in approximately 10% of patients. There can be a pulmonary vessel coursing directly to the mass in approximately 88% of cases (<strong>Figure 9</strong>), coined as the &ldquo;feeding vessel sign.&rdquo; However, this is a nonspecific sign that can be seen in other entities of cavitary disease.<sup>18</sup> Other signs on imaging include a &ldquo;reversed halo sign,&rdquo; which has consolidation surrounding a central ground-glass density.</p>
<p>This disease is an autoimmune disease of uncertain etiology and is treated with immunosuppressive drugs. The nodules and pulmonary disease increase in size and number with progression; however, remission rate is approximately 90% with appropriate treatment.<sup>19</sup> Renal failure is the most common cause of death in this patient population.</p>
<h3>Rheumatoid Arthritis</h3>
<p>Rheumatoid arthritis (RA) is a progressive, systemic autoimmune disorder that is commonly an articular disease, although does present with extra-articular symptoms. The lung is a common site of extra-articular disease and can manifest as airway, parenchymal, or pleural disease.</p>
<p>Necrobiotic rheumatoid nodules of the lung are uncommon and are usually seen in conjunction with a high rheumatoid factor. These nodules are usually large, discrete subpleural nodules, which may develop cavitation. This cavitation can lead to hemoptysis, spontaneous pneumothorax, and the development of a bronchopleural fistula.<sup>20</sup></p>
<p>RA commonly presents with interstitial lung disease, most commonly as UIP and NSIP. There are multiple risk factors for developing RA interstitial lung disease including smoking history, advanced age, high-titer rheumatoid factor, and a family history of RA.<sup>21</sup></p>
<h3>Pyoderma Gangrenosum (PG)</h3>
<p>Pyoderma Gangrenosum is a rare neutrophilic dermatologic disease that occasionally can present with extracutaneous manifestations, which include pulmonary involvement. Etiology is unknown; however, more than 50% of these patients are associated with an underlying systemic disorder such as inflammatory bowel disease, rheumatoid arthritis, or hematological disorders. Pulmonary disease manifestations are rare and are usually diagnosed simultaneously or weeks to years after a cutaneous disease diagnoses.<sup>22</sup></p>
<p>Chest imaging is nonspecific in these patients; however, they can present with pulmonary cystic change and large cavitating nodular lesions or consolidation. The cavitating masses are secondary to nodular lesions that develop central caseation (<strong>Figure 10</strong>) and commonly require histopathological assessment for diagnosis.<sup>23</sup></p>
<h3>Sarcoidosis</h3>
<p>Sarcoidosis is a systemic chronic granulomatous disease characterized by unique noncaseating granulomas in multiple organs. The lungs are involved in more than 90% of these patients.<sup>24</sup> Peak age for presentation is 20 to 30 years and patients generally present with mild cough, dyspnea, or fatigue. This disease should be considered in patients younger than 40 with mild clinical symptoms and bilateral hilar and mediastinal lymphadenopathy on chest x-ray.<sup>24</sup></p>
<p>The greatest morbidity and mortality in this patient population is from thoracic involvement and approximately 20% of these patients will progress to chronic interstitial lung disease. Patients display CT findings of cavitary nodules when central cavitation occurs from ischemic necrosis or angiitis of the nodules.<sup>25</sup> However, the classic pulmonary presentation of sarcoidosis is bilateral hilar and right paratracheal lymphadenopathy with perilymphatic micronodular disease.</p>
<h2>Vascular</h2>
<h3>Septic Emboli</h3>
<p>Infected embolic material can seed the lung parenchyma from an extrapulmonary source through the pulmonary vasculature. This occurs most commonly through infected foreign body material or by less likely etiologies such as infective endocarditis or Lemierre syndrome. <em>Staphylococcus aureus</em> is the most common organism related to foreign body infection and IV drug abuse. This can occur with infected venous catheters, pacemaker wires, or other indwelling catheters.<sup>26</sup> Infective endocarditis of the tricuspid valve is the most commonly affected valve leading to septic embolic disease. Also, Lemierre syndrome is a possible etiology that occurs when acute pharyngotonsillitis leads to jugular vein septic thrombosis, possibly resulting in septic emboli.<sup>27</sup></p>
<p>Imaging findings of pulmonary septic emboli include multiple discrete nodules ranging from 0.5 - 3.5 cm. The nodules are usually bilateral and peripheral with central cavitation (<strong>Figure 11</strong>). Other imaging features seen in this entity include a ground-glass halo surrounding the nodules as well as a &ldquo;feeding vessel sign.&rdquo; Vessels can be seen leading directly to the nodule and are found in 60% to 70% of patients.<sup>27,28</sup></p>
<p>These patients are treated with broad spectrum antibiotics, sometimes up to 6 to 8 weeks in cases of infective endocarditis. Removing the source of infection is imperative for improvement.</p>
<h2>Infection</h2>
<h3>Tuberculosis and Mycobacterium Avium Complex</h3>
<p>A myriad of bacterial, fungal, and parasitic organisms can lead to cavitary lung disease. Among them, the most familiar causative organism is <em>Mycobacterium tuberculosis </em>(TB). The incidence of TB has been decreasing in the US but remains a daunting threat among the immunocompromised population. In addition, immigrants from endemic regions (Asia, Africa, Russia, Eastern Europe and Latin America), those with low incomes and limited access to health care, intravenous drug users, people who live or work in high-risk residential centers (nursing homes, correctional facilities and homeless shelters), and health care workers are still vulnerable to opportunistic organisms.<sup>29</sup></p>
<p>TB is divided into primary vs postprimary tuberculosis. Imaging findings for primary tuberculosis include pulmonary consolidation, effusion, and lymphadenopathy. In postprimary tuberculosis, the most common imaging findings include cavitary lesions in which patients present with fever, night sweats, weight loss, and cough. Cavitary lesions in postprimary TB tend to be in the apical regions with thick irregular walls. Surrounding airspace opacity can also be observed. In cases of superinfection, cavities may present with internal air-fluid levels. Detection of cavitary lesions on imaging do prolong the overall length of treatment (<strong>Figure 12</strong>).<sup>30</sup></p>
<h3>Bacterial Pneumonia/Abscess</h3>
<p>Pulmonary abscesses are most often caused by organisms in the oral cavity, with <em>staphylococci </em>and <em>streptococci </em>the most common. Lung abscesses are divided into acute (&lt; 6 weeks) vs chronic (&gt; 6 weeks). Patients often present with symptoms of fever, chills, fatigue, night sweats, productive cough, and weight loss. Unlike TB, abscesses &gt; 2 cm are almost always found with internal air-fluid levels (<strong>Figure 13</strong>).<sup>31</sup> Lung abscesses are commonly treated with antibiotics for at least 3 to 6 weeks. Moreover, abscesses &gt; 6 cm should be considered for surgical resection or percutaneous transthoracic tube drainage.<sup>32</sup></p>
<h3>Aspergillosis</h3>
<p>Pulmonary aspergillosis is almost exclusively seen in patients with immunodeficiency or with chronic lung disease such as chronic obstructive pulmonary disease&nbsp;(COPD). Many people in the general population are exposed to aspiration of aspergillosis, but only immunodeficient patients will develop clinical symptoms. Types of aspergillosis include aspergilloma, invasive aspergillosis, and semi-invasive aspergillosis. An aspergilloma is when a fungal collection, or &ldquo;fungal ball,&rdquo; develops in a pre-existing cavity and is commonly seen in immunocompetent patients. Semi-invasive aspergillosis is a chronic necrotizing pulmonary aspergillosis, which can develop cavitary lesions (<strong>Figure 14</strong>).<sup>33</sup> Lastly, invasive aspergillosis is seen in severely immunocompromised patients with a rapidly progressive angioinvasive fungal infection and often presents with a pulmonary cavitary lesion and &ldquo;air crescent sign.&rdquo; Typical patient presentation of chronic pulmonary aspergillosis is a middle-aged male with symptoms of weight loss, loss of appetite, productive cough, pleuritic chest pain, and often hemoptysis. Sometimes the cavity may contain an aspergilloma, which is a conglomerate of aspergillosis hyphae, fibrin and cell debris. Treatment options for aspergillosis include azoles followed by inhaled amphotericin B for a prolonged period of 6 to 12 months.</p>
<h2>Trauma</h2>
<h3>Pulmonary Laceration</h3>
<p>Pulmonary laceration, the tearing of lung parenchyma, occurs secondary to traumatic compression, shearing forces, direct injury from rib fractures, or at the site of previously formed pleural adhesions.</p>
<p>Having a round or oval shape with varying number of lesions and sizes, laceration has a highly variable appearance on imaging. Pulmonary laceration is often obscured on chest radiography the first 48 to 72 hours because of surrounding associated pulmonary contusion (<strong>Figures 15 and 16</strong>). CT is more sensitive in detecting pulmonary lacerations offering a more comprehensive assessment of the extent of pulmonary injury and laceration. Air and/or blood may fill in the laceration creating a thin pseudomembrane. Occasionally, active bleeding into a pulmonary laceration can be seen on contrast-enhanced CT. It presents as a linear density, similar to that of the blood pool, forming in or along the periphery of the laceration.<sup>34</sup> Uncommon complications include bronchopleural fistula and abscess, with the former occurring more often in the setting of peripheral lacerations.<sup>34</sup> Healing times vary from weeks to several months for laceration, depending on the severity and associated injury. Having an accurate history during the interpretation of subsequent radiographs or CT scans is critical to prevent mistaking a blood-filled cystic laceration for a neoplasm.<sup>33</sup></p>
<h3>Pneumatocele</h3>
<p>Pneumatoceles are thin-walled cystic spaces in the parenchyma of the lung.<sup>33</sup> It is not uncommon for pneumatoceles to contain fluid, creating an air-fluid level observed on imaging. Infection is the major cause of pneumatoceles, with other etiologies including positive pressure ventilation, hydrocarbon ingestion, and blunt trauma.<sup>34</sup> In the setting of antecedent trauma, pneumatoceles are most often seen as cystic spaces with peripheral ground-glass attenuation. As with pulmonary lacerations, healing may take several weeks, and will often completely resolve. Rare complications include spontaneous rupture with pneumothorax and secondary infection.<sup>35</sup> Rarely, surgical resection of a pneumatocele may be required if the patient has recurrent infections, mass effect, or recurrent rupture with resultant pneumothorax.<sup>34</sup></p>
<h2>Congenital (&ldquo;Youth&rdquo;)</h2>
<h3>Congenital Pulmonary Airway Malformation</h3>
<p>Congenital pulmonary airway malformation (CPAM) includes a spectrum of pulmonary disease that affects varying aspects of the tracheobronchial tree and distal airways. The pathophysiology of CPAM development is controversial, but the entity involves an abnormal mass of pulmonary tissue with differing levels of cystic components that communicate with the tracheobronchial tree. This lesion has normal vascular supply and drainage, which differentiates it from pulmonary sequestrations.<sup>36</sup> The abnormality is usually identified during routine obstetric care, due to increased use of ultrasound, or in children presenting with cough and abnormal chest radiography. It can rarely present in adulthood with recurrent pulmonary infections.</p>
<p>These lesions vary in histological and imaging presentation and have been classified into type 0 through IV. Type 0 is acinar dysplasia or agenesis and is incompatible with survival. Type I is the &ldquo;large-cyst type&rdquo; on imaging and typically affects a single lobe with cyst size 1-10 cm (<strong>Figure 17</strong>). Type II is the &ldquo;small cyst type&rdquo; on imaging, which has small lesions &lt; 2.0 cm. Type III is a solid-appearing lesion with microcysts that coalesce to form a solid-appearing mass on imaging. Type IV disease typically affects a single lobe and has large thin-walled cysts and cannot be readily discernible from type 1 by imaging. Type II and III lesions have a poor prognosis while type I and IV lesions have a much better prognosis.<sup>37</sup></p>
<h3>Bronchopulmonary Sequestration</h3>
<p>A sequestration is a congenital region of abnormal lung tissue that does not connect to the bronchial tree or pulmonary arteries and can present as a cystic lesion on imaging (<strong>Figure 18</strong>). The abnormality commonly presents in the lower lobes, most often the left lower lobe. Often the abnormality presents on chest radiography as a persistent lower-lobe opacity in a patient with recurrent pneumonia. Sequestrations often have a systemic feeding artery arising from the descending aorta, which can be visualized on CT or MR imaging. Sequestrations can also be seen with elements of other congenital pulmonary malformations, including CPAM, with &ldquo;hybrid&rdquo; lesions sometimes visualized.<sup>38</sup> Bronchopulmonary sequestrations can be divided into intralobar and extralobar types.</p>
<p>Intralobar sequestration is more common (approximately 75%), is intrapleural in location, and commonly has pulmonary venous drainage. It usually presents as an isolated anomaly and is often present in older children or adults who present with recurrent pneumonia. Extralobar sequestration is less common (25%) and is extrapleural in location with a separate pleural lining from the normal lung parenchyma. The extralobar sequestration usually has systemic venous drainage.<sup>39</sup> In symptomatic cases, patients often require surgical resection of the abnormal lung tissue.<sup>40</sup></p>
<h3>Bronchogenic Cyst</h3>
<p>Bronchogenic cysts are ventral foregut cysts that occur with abnormal foregut budding between the 26th and 40th day of gestation. They can occur in the mediastinum and pulmonary parenchyma. The mediastinal cysts predominantly occur in the middle or posterior mediastinum and are typically subcarinal extending toward the right hilum. The pulmonary bronchogenic cysts are commonly lower lobe, and more often in the medial aspect. These cysts are well-marginated with thin walls, spherical, and often are simple cysts with no internal debris. They can have internal high attenuation on CT with intraluminal mucoid, hemorrhagic, or viscous contents. They rarely contain internal air or air-fluid levels. CT is often diagnostic of these lesions documenting their fluid-attenuation; however MR, can be useful in patients with indeterminate lesions.<sup>41</sup> These cysts are often asymptomatic, but can rarely present with chest pain, cough or infection. For symptomatic lesions, aspiration or ablation is common, or surgical resection can be performed if they are recurrent and symptomatic.<sup>42</sup></p>
<h2>Conclusion</h2>
<p>When radiologists encounter pulmonary cavitary lesions the differential diagnosis is broad. Pertinent clinical history and imaging findings can help distinguish between the multitude of entities and allow the clinician to expedite appropriate patient management, ultimately improving clinical outcomes.</p>
<h2>References</h2>
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</ol>9822An Overview of Hindfoot Pain and MRI Findings2019-09-27T09:53:05-04:002019-09-27T09:53:05-04:00Dustin Cheney, D.O., Cameron Smith, D.O., Damon Brooks, D.O., Donald von Borstel, D.O.<p>Heel pain is a common complaint among the general population and is present in 1 of 8 individuals, particularly those over age 50.<sup>1</sup> Additionally, heel pain is one of the most prevalent complaints necessitating referral to a foot specialist. There are multiple etiologies for heel pain, which generally originates from 6 major anatomic structures: the plantar fascia, calcaneus, tarsal tunnel, tendons, bursae, and plantar fat pad.<sup>2</sup></p>
<p>This article will review the differential diagnosis for hindfoot pain as well as discuss pertinent MRI findings for each condition.</p>
<h2>Plantar Fascia</h2>
<p>The plantar fascia is a fibrous aponeurosis that arises along the medial calcaneal tuberosity.<sup>2</sup> From the calcaneus, the plantar fascia divides into the medial, central, and lateral components (<strong>Figure 1</strong>).</p>
<p>The central band is the largest, adhering to the undersurface of the flexor digitorum brevis. At the midsole, the central band divides into 5 superficial and deep components extending toward the digits as the flexor tendons. This, along with the medial and lateral marginal superficial tracts, inserts onto each proximal phalanx. The plantar fascia plays a significant role in longitudinal arch support.</p>
<h2>Plantar Fasciitis</h2>
<p>Plantar fasciitis is one of the more common causes of plantar heel pain.<sup>3,4</sup> Plantar fasciitis is related to microtrauma at the os calcis attachment and can result from repetitive trauma, enthesopathy, pes planus, pes cavus, or heel cord contractures. Stress-related trauma is the most common etiology and usually affects obese middle-age or elderly patients.<sup>5</sup> Imaging-related findings for fasciitis include thickening of the plantar fascia (&gt; 6 mm) at the proximal attachment and high-signal intensity on T2-weighted sequences with low to intermediate signal on T1-weighted sequences (<strong>Figure 2</strong>).<sup>6</sup></p>
<h3>Plantar Fascia Tear</h3>
<p>A fascial tear is usually traumatic in etiology with sudden onset and localized tenderness. Fascial tears are comonly seen in running or jumping athletes.<sup>7</sup> Imaging findings of acute tears will demonstrate a partial or full-thickness defect of the fascia with focal hyperintense signal on T2-weighted or short tau inversion recovery (STIR) sequences.<sup>7</sup> Peri-fascial fluid-like signal can also be seen (<strong>Figure 3</strong>).</p>
<h3>Plantar Fibromatosis</h3>
<p>Plantar fibromatosis (Ledderhose disease) is a fibroproliferative disorder in which benign fibrous nodules develop within the plantar fascia.<sup>8</sup> Plantar fibromatosis can be associated with many other fibroproliferative disorders such as Dupuytren disease and Peyronie disease.<sup>9</sup> Plantar fibromatosis usually involves the more distal fascia and the central or medial bands. Imaging findings of plantar fibromatosis show nodular-thickening of the nonweight-bearing portions of the plantar fascia, which is hypointense on both T1- and proton density (PD)-weighted sequences (<strong>Figure 4</strong>). Hyperintense signal of the adjacent subcutaneous soft-tissues on T2- or PD-weighted sequences can also be seen.</p>
<p>There are multiple treatment options for plantar fibromatosis, which include surgical resection, radiation, and chemotherapy, used alone or in combination. The treatment is determined based on disease aggressiveness, patient age, and the risk of disability with resection. Surgical resection is the most common treatment; however, recurrence rates are high and can be deforming, even requiring amputation in some cases. If there is a possibility of functional loss, marginal excision and postoperative radiation therapy can be used. In the case of severe neurovascular or significant limb involvement, chemotherapy and radiation are often the sole option for treatment. Chemotherapy alone can also be used in young children to avoid disfiguring surgery and complications of radiation.<sup>8</sup></p>
<h2>Calcaneus</h2>
<p>The calcaneus is responsible for significant axial load-bearing forces and is the most commonly fractured tarsal bone, responsible for up to 60% of all tarsal bone fractures in adults.<sup>10</sup></p>
<h3>Calcaneal Stress Fracture</h3>
<p>Most stress fractures result from repetitive activity as opposed to direct trauma. Thus, calcaneal stress fractures are common in patients undergoing a new occupation or repetitive motions (ie, military recruits or runners). Stress fractures are further classified as fatigue fracture (overuse in normal bone) or insufficiency fracture (normal use in abnormal bone).<sup>2</sup> Conditions related to insufficiency fractures include those that weaken the bone integrity such as metabolic disorders, inflammatory conditions, bone dysplasias, and neurological disorders.<sup>11</sup></p>
<p>Calcaneal stress fractures are a cause of hindfoot pain that is commonly not visualized or radiographically occult, especially in the early stages. Reported radiographic sensitivity for the diagnosis of lower extremity stress fractures ranges from 12% to 56% with a specificity of 88% to 96%. MRI sensitivity and specificity for detecting stress fracture can be as high as 99% and 97%, respectively.<sup>12</sup> MRI demonstrates linear hypointense signal in bone marrow on T1-weighted images, which extends to the cortex with surrounding increased marrow signal on T2-weighted and STIR sequences (<strong>Figure 5</strong>)<sup>13</sup> Calcaneal stress fractures are more common in the posterior calcaneus.</p>
<h2>Tarsal Tunnel and Nerve Entrapment</h2>
<h3>Tarsal Tunnel Syndrome</h3>
<p>The tarsal tunnel is a fibro-osseous canal in the medial aspect of the ankle, which is a common location for compression and entrapment of neurovascular structures. The tarsal tunnel contains the tibialis posterior (TP) tendon, flexor digitorum longus (FDL) tendon, posterior tibial artery/vein and tibial nerve, and the flexor hallucis longus (FHL) tendon. The tarsal tunnel is created by the medial talar wall, the sustentaculum tali, and the medial calcaneal wall. The flexor retinaculum forms the roof of the tarsal tunnel (<strong>Figure 6</strong>).<sup>2</sup></p>
<p>Tarsal tunnel syndrome results from neuropathic entrapment or compression within the tunnel. The posterior tibial nerve and its branches can be compressed as it passes through the fibro-osseous tunnel, deep to the flexor retinaculum. Patients suffering from tarsal tunnel syndrome generally experience pain and sensory deficits.<sup>14</sup></p>
<p>Numerous etiologies can cause tarsal tunnel syndrome with up to 40% of cases being idiopathic, and less likely etiologies including ganglion cysts, tenosynovitis, varicosities, and osseous deformities.<sup>2</sup> The patient&rsquo;s symptoms can suggest the location of nerve entrapment as well as the branch of the posterior tibial nerve that is involved. For example, medial plantar nerve entrapment can occur at the tarsal tunnel or distally. These patients usually present with heel or arch pain. The lateral plantar nerve is also commonly entrapped at the tarsal tunnel or distal to the tarsal tunnel with loss of sensation along the distal third of the foot.</p>
<p>Imaging findings of tarsal tunnel syndrome depend on underlying etiology. Space-occupying lesions are well depicted on MRI, such as varicosities (<strong>Figure 7</strong>) and a large aneurysmal bone cyst of the talus causing mass effect on the tarsal tunnel (<strong>Figure 8</strong>).</p>
<h3>Baxter Neuropathy</h3>
<p>Baxter neuropathy is a syndrome caused by the entrapment of the inferior calcaneal nerve.<sup>15</sup> The inferior calcaneal nerve is the first branch of the lateral calcaneal nerve, which if entrapped, can result in chronic heel pain often mimicking plantar fasciitis. Entrapment of the inferior calcaneal nerve occurs at 3 locations in the hindfoot: the medial border of the quadratus plantae muscle, along the fascial edge of an enlarged/hypertrophied abductor hallucis muscle, and most commonly at the medial calcaneal tuberosity. Imaging findings are usually related to denervation with increased signal intensity or atrophy of the intrinsic muscles of the foot. Incidental atrophy of the abductor digiti minimi likely reflects a prior clinically missed entrapment (<strong>Figure 9</strong>) and is not an uncommon finding.<sup>16,17</sup></p>
<h2>Tendons</h2>
<p>Tendons normally have a homogenous hypointense signal on all MRI sequences within the hindfoot.<sup>18</sup> The main tendons of the hindfoot include the peroneus longus, peroneus brevis, Achilles, posterior tibial, FDL, and FHL tendons. &nbsp;</p>
<h3>Achilles Tendon</h3>
<p>The Achilles tendon is formed by the communion of the gastrocnemius and soleus muscles. The tendon inserts at the posterior calcaneus, os calcis. The Achilles tendon normally has a concave anterior and posterior convex contour and has low signal intensity on all sequences. Thickness of the tendon averages 6 mm.<sup>19,20</sup> A common normal finding is linear or punctate increased signal intensity on low echo time (TE) sequences, usually more anterior within the tendon. This signal represents normal fascicular anatomy but can be mistaken for interstitial tears, therefore knowing this common appearance and location is imperative (<strong>Figure 10</strong>).<sup>21,22 </sup>Achilles tendinopathy or tendinosis can be insertional or mid-substance. Non-insertional tendinosis is usually acute in onset and often proximal to the retrocalcaneal bursa. This entity usually occurs in older individuals who are less active and overweight.<sup>23,24</sup> Insertional tendinopathy results from repetitive trauma and micro tears which usually present with weight-bearing pain in less athletic or active individuals and more commonly associated with running and jumping.<sup>2,23,24</sup> Imaging findings on MR will demonstrate focal or fusiform thickening with diffuse or linear low to intermediate signal on fluid sensitive sequences (<strong>Figures 11 and 12</strong>). The Achilles tendon is unique as it does not have a true synovial sheath. However, it does have a thin sheath-like structure surrounding the tendon that is separated from the tendon by a lubricating layer of mucopolysaccharides. This structure is called the paratenon. Similar to tenosynovitis, with overuse the paratenon can become inflamed and cause pain. This is called paratenonitis (<strong>Figure 11</strong>).</p>
<p>Achilles ruptures, or complete tears, usually occur from 25-40 years of age. Activities that require dorsiflexed position while running or jumping are at a greater risk. Complete tears will demonstrate a T2-hyperintense signal defect of the tendon (<strong>Figure 13</strong>). Partial or complete retraction of fibers can be seen, depending on the degree of tearing. Chronic tendon pathology may lack intrasubstance signal but can be diffuse or focally thickened.<sup>25</sup></p>
<h3>Tibialis Posterior, Flexor Digitorum Longus, and Flexor Hallucis Longus Tendons</h3>
<p>The FDL and FHL tendons course through a shallow groove in the posteromedial aspect of the talus and continue under the sustentaculum tali. On the plantar aspect of the heel, the FHL tendon crosses deep to the FDL tendon at the Master Knot of Henry, before their insertion on the base of the great toe and lesser distal phalanges, respectively.<sup>26</sup> The TP tendon originates at the posterior tibia, fibula, and interosseous membrane. From its origin it courses along the deep posterior compartment of the lower leg, through the tarsal tunnel, under and around the medial malleolus and into its insertion at the plantar aspect of the navicular, cuneiforms, and metatarsal bases.<sup>27</sup></p>
<p>The TP, FDL, and FHL tendons are prone to tendonitis and tenosynovitis, which results in a painful posteromedial heel. These findings are more commonly seen in athletes performing repetitive forceful push off motion with the forefoot. Tenosynovitis is demonstrated by increased fluid-like signal intensity on T2-weighted sequences distending the tendon sheath (<strong>Figures 14 and 15</strong>).<sup>2</sup> However, it is important to note that fluid in the FHL tendon sheath may be considered physiologic if similar to the volume of intraarticular fluid, as these structures often communicate.</p>
<h3>Peroneus Longus and Brevis Tendons</h3>
<p>The peroneus longus and brevis tendons course along a groove posterior to the fibula in the lateral ankle and curve anteroinferiorly along the undersurface of the foot. The peroneus longus inserts on the medial cuneiform and the base of the first metatarsal. The peroneus brevis inserts on the base of the fifth metatarsal. The peroneal tendons are also susceptible to tendonitis and tenosynovitis. Repetitive acute tenosynovitis can result in fibrous scar formation in the tendinous sheath, known as stenosing tenosynovitis. Imaging findings of stenosing tenosynovitis will demonstrate an intermediate signal intensity rind surrounding the tendon on both the T1- and T2-weighted sequences <strong>(Figures 16 and 17</strong>).</p>
<h2>Bursae</h2>
<p>There are two bursae of the hindfoot lying near the insertion of the Achilles tendon to the calcaneus. The retrocalcaneal bursa is located between the Achilles tendon insertion and the calcaneus. The retroachilles bursa (or subcutaneous calcaneal bursa) is situated between the skin and the Achilles tendon.<sup>28</sup> On MRI a normal retrocalcaneal bursa is usually present and measures &lt; 6 mm in the transverse plane and 1 mm in the anterior-posterior dimension.<sup>29</sup> When these bursae become inflamed, they can generally be seen as uninterrupted MRI fluid-like signal in the expected locations of the bursae.</p>
<h3>Haglund Syndrome</h3>
<p>A Haglund deformity is a prominent bursal bony projection of the calcaneus, which can be a normal anatomical structure or associated with other findings.<sup>30</sup> Haglund syndrome is the result of both soft tissue and osseous abnormalities consisting of a Haglund deformity, insertional tendinopathy, and pre-Achilles and/or retrocalcaneal bursitis. This entity is commonly associated with low-back or high-heel shoes.<sup>30</sup> The imaging findings of Haglund syndrome include a prominent posterosuperior tuberosity of the calcaneus with or without increased marrow signal on the fluid-sensitive sequences, fluid-like signal within the pre-Achilles or retro-Achilles bursa, increased signal on T2/STIR sequences in the Kager (pre-Achilles) fat pad, and insertional tendinopathy of the Achilles tendon (<strong>Figure 18</strong>).</p>
<h3>Retroachilles and Retrocalcaneal Bursitis</h3>
<p>Bursitis in the retroachilles and retrocalcaneal bursa is most commonly a manifestation of Achilles pathology but can also occur as a separate entity. One of the more common causes of retroachilles and retrocalcaneal bursitis is repetitive trauma or friction. Bursitis can also be seen in the setting of rheumatoid arthritis and seronegative spondyloarthropathies. The retrocalcaneal bursa should measure &lt; 1-2 mm in anteroposterior dimension. If enlarged, it may represent disease, especially if surrounding edematous changes are present. The subcutaneous fat should be seen between the Achilles tendon and the skin. If this fat cannot be seen on MRI, a blister or retro-Achilles bursitis may be present. In particular, retro-Achilles bursitis is distinguished by edematous changes without mass effect on the skin.<sup>2</sup></p>
<h2>Plantar Fat Pad</h2>
<p>The heel fat pad is composed of elastic fibrous septae with closely packed fat cells that act as a shock-absorber for the heel. Several plantar fat pad pathologies such as ulcers, abrasions and contusions can be identified with a detailed history and physical examination. However, the use of MRI is sometimes required to provide a differential diagnosis for heel pad abnormalities that cannot be explained clinically. Numerous causes of heel pain can arise from the fat pad, including infection, trauma (rupturing of the septa), neoplasm, inflammatory conditions, and rheumatoid nodules.</p>
<p>Rheumatoid nodules of the heel pad occur in 20% of patients who test positive for rheumatoid factor.<sup>2</sup> Rheumatoid nodules usually develop on the pressure areas in the heel, but may occur near the Achilles tendon insertion. Imaging findings are related to their histologic composition. Solid nodules are composed of chronic inflammatory cells and usually show decreased signal intensity on T1- and T2-weighted sequences with postcontrast enhancement. Nodules can have central necrosis with increased signal intensity on T2-weighted sequences and peripheral enhancement (<strong>Figure 19</strong>).<sup>31</sup></p>
<h2>Conclusion</h2>
<p>Heel pain is a common musculoskeletal complaint for presentation to primary care or a foot specialist, and the specific etiology is often difficult to ascertain clinically. The heel is a complex area to assess with numerous sources of pain. However, compartmentalizing the heel into different anatomic structures and understanding the imaging findings and differential diagnoses for each location will help guide the clinician to a more accurate diagnosis and earlier treatment.</p>
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<li>Stress fractures in the foot and ankle. Radsource. http://radsource.us/stress-fractures-foot-ankle/. Published August 1, 2016. Accessed January 3, 2018.</li>
<li>Donovan A, Rosenberg ZS, Cavalcanti CF. MR imaging of entrapment neuropathies of the lower extremity. Radiographics 2010;30(4):1001-1019.</li>
<li>Baxter&rsquo;s Nerve (First Branch of the Lateral Plantar Nerve) Impingement - Radsource. Radsource. http://radsource.us/baxters-nerve/. Published August 1, 2012. Accessed November 27, 2018.</li>
<li>Schmid DT, Hodler J, Mengiardi B, Pfirrmann CWA, Espinosa N, Zanetti M. Fatty muscle atrophy: prevalence in the hindfoot muscles on MR images of asymptomatic volunteers and patients with foot pain. Radiology 2009;253(1):160-166.</li>
<li>Recht MP, Grooff P, Ilaslan H, Recht HS, Sferra J, Donley BG. Selective atrophy of the abductor digiti quinti: an MRI study. Am J Roentgenol 2007;189(3):W123-W127.</li>
<li>Hodgson RJ, O&rsquo;Connor PJ, Grainger AJ. Tendon and ligament imaging. Br J Radiol 2012;85(1016): 1157-1172.</li>
<li>Achilles Tendon Pathology - Radsource. Radsource. http://radsource.us/achilles-tendon-pathology/. Published January 3, 2017. Accessed January 9, 2018.</li>
<li>Koivunen-Niemel&auml; T, Parkkola K. Anatomy of the Achilles tendon (tendo calcaneus) with respect to tendon thickness measurements. Surg Radiol Anat 1995;17(3):263-268.</li>
<li>Mantel D, Flautre B, Bastian D, Delforge PM, Delvalle A, Leclet H. [Structural MRI study of the Achilles tendon. Correlation with microanatomy and histology]. J Radiol 1996;77(4):261-265.</li>
<li>Schweitzer ME, Karasick D. MR imaging of disorders of the Achilles tendon. Am J Roentgenol 2000;175(3):613-625.</li>
<li>Irwin TA. Current concepts review: insertional achilles tendinopathy. Foot Ankle Int 2010;31(10):933-939.</li>
<li>Chimenti RL, Cychosz CC, Hall MM, Phisitkul P. Current concepts review update: insertional Achilles tendinopathy. Foot Ankle Int 2017;38(10):1160-1169.</li>
<li>Lawrence DA, Rolen MF, Morshed KA, Moukaddam H. MRI of heel pain. Am J Roentgenol 2013;200(4):845-855.</li>
<li>Stoller DW. Magnetic Resonance Imaging in Orthopaedics and Sports Medicine. Philadelphia, PA: Lippincott Williams &amp; Wilkins; 2007.</li>
<li>Thompson JC, Netter FH. Netter&rsquo;s Concise Atlas of Orthopaedic Anatomy. Teterboro, NJ: Icon Learning Systems; 2002.</li>
<li>Pierre-Jerome C, Moncayo V, Terk MR. MRI of the Achilles tendon: a comprehensive review of the anatomy, biomechanics, and imaging of overuse tendinopathies. Acta Radiol. 2010;51(4):438-454.</li>
<li>Bottger BA, Schweitzer ME, El-Noueam KI, Desai M. MR imaging of the normal and abnormal retrocalcaneal bursae. Am J Roentgenol 1998;170(5):1239-1241.</li>
<li>Pavlov H, Heneghan MA, Hersh A, Goldman AB, Vigorita V. The Haglund syndrome: initial and differential diagnosis. Radiology 1982;144(1):83-88.</li>
<li>el-Noueam KI, Giuliano V, Schweitzer ME, O&rsquo;Hara BJ. Rheumatoid nodules: MR/pathological correlation. J Comput Assist Tomogr 1997;21(5):796-799.</li>
</ol>9820Carpal Instability: Clarification of the Most Common Etiologies and Imaging Findings2019-09-27T09:43:45-04:002019-09-27T09:43:45-04:00<p>Intrinsic ligament injuries of the wrist are common with varying degrees of scapholunate ligament tears occurring in more than one-third of involved wrists.<sup>1</sup> A fundamental understanding of wrist anatomy and common patterns of injury help increase early detection and proper management of carpal instability.</p>
<p>Plain film radiographs offer an adequate cursory evaluation of carpal instability and exclude other entities that may mimic instability such as fracture. Additionally, radiographs display the alignment of the wrist and carpal bones (<strong>Figure 1</strong>). Ensuring proper positioning of the wrist (ie, frontal and lateral projections) allows for appropriate assessment of the joint spaces and carpal arcs<sup>2</sup> as well as initial screening for acute fracture or dislocation.</p>
<p>MRI provides a more thorough evaluation for underlying pathology and associated sequelae<sup>3,4</sup> (<strong>Figures 2</strong>). Incorporating an appropriate protocol for MRI of the wrist (<strong>Table 1 and 2</strong>) offers exquisite detail of the bones, cartilage, ligaments, tendons and nerves. At the authors&rsquo; institution, this includes axial proton density-weighted sequences with and without fat saturation, coronal T1-weighted images, coronal proton density-weighted images with fat saturation, and coronal 3D double echo steady state as well as sagittal proton density-weighted images with fat saturation.</p>
<h2>Carpal Instability Classification</h2>
<p>The first step toward accurate wrist radiography is to ensure proper anatomic positioning. In the frontal projection, the carpal bones should be parallel with undisrupted arches, normal in shape (implying normal tilt and axis), and equally spaced. The shape of the lunate, capitate, and scaphoid requires close attention as they are the most common carpal bones to be malaligned.<sup>5</sup> The lateral projection is also critical, particularly in determining the alignment and/or angulation of the capitate, lunate, scaphoid and radius, and is critical in evaluating intercalated segment instability.<sup>6</sup></p>
<p>Overall classification of carpal instability is separated into 4 large groups (<strong>Table 3</strong>).<sup>3</sup> Within this classification scheme, the most common etiologies include dorsal intercarpal (DIC) and dorsal perilunate (DPL) dislocations. These common clinical entities have specific radiographic and MRI characteristics.</p>
<h2>Carpal Instability Dissociative</h2>
<p>These injuries include scapholunate dissociation, scapholunate advanced collapse, scaphoid nonunion advanced collapse, and the less common lunotriquetral dislocation, which can range from incomplete tears to complete dissociation.<sup>7</sup> These entities can be adequately evaluated and diagnosed with radiography; however, specific ligamentous injuries and extent of degenerative disease is better appreciated with MRI.</p>
<p>Dorsal intercalated segment instability (DISI) and volar intercalated segment instability (VISI) are the most common patterns of carpal instability and are associated with scapholunate and lunotriquetral ligament injuries, respectively.<sup>8</sup> They can be suggested on radiographic evaluation with typical findings and abnormal angulation of the carpal bones, but are not always evident even in the setting of ligamentous injury, which is better seen by MRI.<sup>9</sup> Dorsal perilunate dislocations can be separated into 4 stages of injury with progressive perilunate instability occurring secondary to ligamentous injuries. These stages of instability include scapholunate dissociation, perilunate dislocation, midcarpal dislocation, and lunate dislocation. Each stage has a differing radiographic appearance allowing accurate diagnosis with specific ligamentous injury, well visualized by MRI.<sup>10</sup></p>
<p>Carpal instability dissociative (CID) involves injury within or between bones of the same carpal row. Most commonly, this instability pattern occurs in the proximal carpal row as a result of scapholunate or lunotriquetral ligament injury and the different specific type of injuries include scapholunate dissociation, dorsal intercalated segment instability, scapholunate advanced collapse, scaphoid nonunion advanced collapse, and lunotriquetral dislocation.<sup>11</sup></p>
<h3>Scapholunate Dissociation</h3>
<p>Scapholunate dissociation (SLD) is disruption of the ligamentous connection between the scaphoid and lunate (<strong>Figures 3</strong>). This is seen on radiography as diastasis of the scapholunate interval with a gap of &gt; 3mm (&ldquo;Terry Thomas&rdquo; or &ldquo;David Letterman&rdquo; sign).<sup>12</sup> This is the most frequent carpal instability pattern and can be isolated or associated with scaphoid fractures.</p>
<h3>Dorsal Intercalated Segment Instability</h3>
<p>Dorsal intercalated segment instability (DISI) involves injury to the scapholunate ligament and concomitant failure of the scaphoid stabilizers, which often results in permanent carpal malalignment. In this pattern, the lunate is dorsiflexed and the scaphoid is tilted volarly with a scapholunate angle &gt; 60˚ (normal range is 30˚ to 60˚) and a capitolunate angle &gt; 30̊, as measured on a lateral radiograph (<strong>Figure 4</strong>).<sup>13</sup></p>
<h3>Scapholunate Advanced Collapse</h3>
<p>Scapholunate advanced collapse, commonly abbreviated as &ldquo;SLAC wrist,&rdquo; occurs with degenerative joint disease centered at the radioscaphoid joint from chronic SLD. There are 3 progressive stages of SLAC wrist: stage I, which involves radial styloid and scaphoid degeneration; stage II (<strong>Figure 5</strong>), which involves degeneration between the scaphoid and the entire scaphoid facet of the radius; and stage III (<strong>Figure 6</strong>), which involves degeneration between the capitate and lunate.<sup>13</sup> The hallmark of a SLAC wrist is scapholunate ligament tear and progressive scapholunate interval widening.</p>
<h3>Scaphoid Nonunion Advanced Collapse</h3>
<p>Scaphoid nonunion advanced collapse, commonly abbreviated as a &ldquo;SNAC wrist,&rdquo; occurs with a scaphoid fracture (particularly nonunion fractures) with distal scaphoid fracture segment flexion and results in abnormal radioscaphoid articulation and degeneration (<strong>Figure 7</strong>). The hallmark of SNAC wrist is post-traumatic arthritis and carpal collapse following a nonunion scaphoid fracture.<sup>14</sup></p>
<h3>Lunotriquetral Dissociation</h3>
<p>Lunotriquetral dissociation can occur following trauma or ulnocarpal abutment associated with triangular fibrocartilage complex pathology.<sup>7</sup> Injury to the lunotriquetral ligament results in volar intercalated segment instability (VISI), in which the lunate is flexed volarly secondary to the scaphoid flexion. In this pattern, the radiographic findings demonstrate a capitolunate angle &gt; 30˚ and a scapholunate angle &gt; 30˚.<sup>13</sup></p>
<h2>Carpal Instability Nondissociative</h2>
<p>Carpal instability nondissociative (CIND) refers to dysfunction between the radius and first carpal row (radiocarpal) or between the first carpal row and the second carpal row (midcarpal). This dysfunction can involve either the intrinsic or extrinsic ligaments of the wrist; however, there is no disruption between carpal bones in the same row, as in CID.<sup>15</sup> In this pattern, the individual carpal bones in each carpal row maintain their normal anatomic relationship with each other. As a result, the carpal rows and arcs maintain their intrinsic morphology and positioning.</p>
<p>Ulnar translocation occurs the extrinsic ligaments of the wrist are torn; resulting in ulnar shift of the proximal carpal row. Type I ulnar translocation involves tearing of the radioscaphoid and radioscaphocapitate extrinsic ligaments with resultant widening of the radioscaphoid interval and ulnar shift of the entire proximal carpal row (<strong>Figure 8</strong>). In type II ulnar translocation, the radioscaphoid joint is maintained with ulnar shift of the remaining proximal carpal row.<sup>16</sup></p>
<h2>Carpal Instability Complex</h2>
<p>Carpal instability complex (CIC) refers to carpal derangement involving an altered relationship between bones in the same carpal row and between the proximal and distal carpal rows (ie, both CID and CIND injuries).<sup>17</sup> There are 5 subgroups of CIC (<strong>Table 4</strong>), with the more common groups 1 and 2 reviewed below.</p>
<p>Dorsal perilunate dislocations are ligamentous lesser arc injuries within the carpal instability complex class of injuries. There are 4 stages of progressive perilunate instability involving ligamentous injuries surrounding the lunate:<sup>18</sup></p>
<p><strong>Stage I: </strong>Scapholunate dissociation, which is defined by disruption of the dorsal scapholunate ligament when torque on the scapholunate ligament reaches threshold. Ligamentous injury is well visualized by MRI.</p>
<p><strong>Stage II:</strong> Perilunate dislocation, which is when the scaphoid-capitate complex dislocates dorsal to the lunate. The extent of dorsal translation is determined by laxity of the radioscaphocapitate extrinsic ligament. Radiographic findings include dorsal displacement of the capitate in relation to the lunate while alignment of the lunate with the distal radius is maintained (<strong>Figure 9</strong>).</p>
<p><strong>Stage III:</strong> Midcarpal dislocation involves progressive carpal hyperextension, which pulls the triquetrum into abnormal extension. This leads to tearing of the lunotriquetral ligament with possible avulsion injury of the triquetrum, leaving only the short radiolunate and volar ulnolunate ligaments as stabilizers. This injury is best evaluated by MRI. Radiographic findings include abnormal alignment of the lunate and radius (<strong>Figure 10</strong>).</p>
<p><strong>Stage IV:</strong> Lunate dislocation, in which the capitate is pulled proximal and volar by the intact radioscaphocapitate extrinsic ligament causing the capitate to push the lunate volarly. Radiographic findings demonstrate maintained alignment of the capitate with the radius and volar tilting and displacement of the lunate in relation to the radius. There is increased volar tilt of the lunate compared to stage III (<strong>Figure 11</strong>).</p>
<p>Dorsal perilunate fracture-dislocation involves perilunate dislocation secondary to carpal bone fracture (eg, scaphoid, capitate, hamate, or triquetrum). The most common subtype is the trans-scaphoid perilunate dislocation (<strong>Figure 12</strong>).</p>
<h2>Carpal Instability Adaptive</h2>
<p>Carpal instability adaptive (CIA) occurs when the carpal rows adapt and change their angle in response to pathology or abnormal anatomy near the wrist.<sup>5</sup> CIA results most commonly from abnormal tilt of the radius (ie, Madelung&rsquo;s deformity or fracture malunion). Intrinsic ligament injury should be excluded with MRI of the wrist.</p>
<h2>Conclusion</h2>
<p>Carpal instability is a significant source of chronic pain and disability. The wrist is a highly organized group of ligaments and bones that normally allow for stable transition of strength, dexterity, and fine-motor control from the forearm to the hand&mdash;functions that are progressively limited as carpal instability worsens. Therefore, discerning the most common etiologies of instability and their imaging findings is important to avoid increased morbidity and degenerative disease that can result from misdiagnosis. While carpal instability is recognizable on plain-film radiography, MRI offers superior visualization of the extent of carpal instability, specific ligamentous injuries, and its long-term sequelae.</p>
<h2>References</h2>
<ol>
<li>Michelotti BF, Adkinson JM, Chung KC. Chronic scapholunate ligament injury: techniques in repair and reconstruction. Hand Clin 2015;31(3):437-449.</li>
<li>Taleisnik J. Current concepts review. Carpal instability. J Bone Joint Surg Am 1988;70(8):1262-1268.</li>
<li>Carpal Instability &ndash; MRI Web Clinic &ndash; June 2012. http://radsource.us/carpal-instability/. Accessed September 18, 2018.</li>
<li>Caggiano N, Matullo KS. Carpal instability of the wrist. Orthop Clin North Am 2014;45(1):129-140.</li>
<li>Lee DJ, Elfar JC. Carpal ligament injuries, pathomechanics, and classification. Hand Clin 2015;31(3):389-398.</li>
<li>Kani KK, Mulcahy H, Chew FS. Understanding carpal instability: a radiographic perspective. Skeletal Radiol 2016;45(8):1031-1043.</li>
<li>Shin AY, Weinstein LP, Berger RA, Bishop AT. Treatment of isolated injuries of the lunotriquetral ligament. A comparison of arthrodesis, ligament reconstruction and ligament repair. J Bone Joint Surg Br 2001;83(7):1023-1028.</li>
<li>Wright TW, Dobyns JH, Linscheid RL, Macksoud W, Siegert J. Carpal instability non-dissociative. J Hand Surg Br 1994;19(6):763-773.</li>
<li>Lichtman DM, Wroten ES. Understanding midcarpal instability. J Hand Surg Am 2006;31(3):491-498.</li>
<li>Niacaris T, Ming BW, Lichtman DM. Midcarpal Instability: A comprehensive review and update. Hand Clin 2015;31(3):487-493.</li>
<li>Ramamurthy NK, Chojnowski AJ, Toms AP. Imaging in carpal instability. J Hand Surg Eur Vol. 2016;41(1):22-34.</li>
<li>Chim H, Moran SL. Wrist essentials: the diagnosis and management of scapholunate ligament injuries. Plast Reconstr Surg 2014;134(2):312e-322e.</li>
<li>Pomeranz SJ, Salazar P. Scapholunate advanced collapse. J Surg Orthop Adv 2015;24(2):140-143.</li>
<li>Shah CM, Stern PJ. Scapholunate advanced collapse (SLAC) and scaphoid nonunion advanced collapse (SNAC) wrist arthritis. Curr Rev Musculoskelet Med 2013;6(1):9-17.</li>
<li>Wolfe SW, Garcia-Elias M, Kitay A. Carpal instability nondissociative. J Am Acad Orthop Surg. 2012;20(9):575-585.</li>
<li>Toms AP, Chojnowski A, Cahir JG. Midcarpal instability: a radiological perspective. Skeletal Radiol 2011;40(5):533-541.</li>
<li>Carlsen BT, Shin AY. Wrist instability. Scand J Surg 2008;97(4):324-332.</li>
<li>Mayfield JK. Wrist ligamentous anatomy and pathogenesis of carpal instability. Orthop Clin North Am 1984;15(2):209-216.</li>
</ol>9790Diaphragmatic Hernia in a Patient with Chest Trauma2019-06-20T11:07:05-04:002019-06-20T11:07:05-04:00Nadia Lushina, M.D., Niveditha Thangaraj, M.D., Christopher Brown, M.D., Nancy Mohsen, M.D.<h2>Case Presentation</h2>
<p>A 27-year-old man was brought to the emergency department following a major motor vehicle collision as an unrestrained driver. On physical examination, he was in severe respiratory distress and had reduced breath sounds, palpable left rib fractures, and crepitus over the left chest. An initial chest radiograph was performed (<strong>Figure 1</strong>) followed by CT (<strong>Figures 2, 3</strong>).</p>
<h2>Key Imaging Findings</h2>
<p>&gt;A left diaphragmatic hernia in the setting of major blunt chest trauma</p>
<h2>Differential Diagnosis</h2>
<p>Traumatic diaphragmatic rupture</p>
<p>Bochdalek diaphragmatic hernia</p>
<p>Morgagni diaphragmatic hernia</p>
<p>Hiatal hernia</p>
<h2>Discussion</h2>
<p>Diaphragmatic hernias are common and encountered routinely in chest imaging. However, traumatic rupture is less common compared to the ubiquitous hiatal hernia.<sup>1</sup> An initial chest radiograph demonstrated nonspecific opacities in the left base. These abnormalities were further characterized on subsequent CT that revealed the opacities on radiography to represent a combination of the herniated abdominal contents in the inferior left hemi-thorax as well as pleural fluid (blood) and airspace disease (contusion and atelectasis).</p>
<p>The differential for this case includes traumatic and nontraumatic causes of diaphragmatic hernias and includes the eponymous Bochdalek and Morgagni hernias, a hiatal hernia, and traumatic diaphragmatic rupture. In addition to the location and CT appearance of the hernia, the history and presence of other significant traumatic pathology are key considerations when evaluating the diagnostic possibilities.</p>
<h2>Differential Diagnosis</h2>
<h3>Traumatic Diaphragmatic Rupture</h3>
<p>Rupture of the diaphragm is not common, but is identified in a small percent of patients with blunt trauma, with motor vehicles accidents being the most common cause.<sup>1</sup> Penetrating injuries are more common causes of diaphragmatic injury.<sup>1</sup> Traumatic diaphragmatic rupture from blunt trauma occurs more frequently in the posterolateral aspect of the hemi-diaphragms at sites thought to be relatively weaker structurally.<sup>1,2</sup> It is more commonly diagnosed on the left side with a variety of reasons hypothesized for the disparity in laterality including the liver providing a degree of protection to the right hemi-diaphragm.<sup>1-3</sup></p>
<p>Traumatic diaphragmatic rupture is rarely an isolated CT finding, with other traumatic findings in the thorax such as a rib fracture(s), effusions, and pneumothoraces also present in the vast majority of cases.<sup>1</sup> Diaphragmatic rupture in the setting of blunt trauma often results in larger diaphragmatic defects (often &gt; 10 cm) compared to penetrating trauma, leading to a larger defect for upward herniation of abdominal organs due to negative intrathoracic pressure.<sup>1-3</sup></p>
<p>Diaphragmatic rupture may occasionally be suggested on chest radiography. Radiographic findings include diaphragmatic elevation, intrathoracic stomach bubble or other intrathoracic bowel, and abnormal location of an oro- or nasogastric tube tip.<sup>2,3</sup> CT is more likely to delineate a traumatic diaphragmatic rupture due to the greater anatomic detail compared to chest radiographs. With modern scanners, the diaphragm and the defect will likely be directly visualized with coronal and sagittal reconstructions aiding visualization. In addition to directly identifying the diaphragmatic defect, other CT signs of diaphragmatic rupture include thickening of the remaining diaphragm due to blood and/or muscle retraction, the &ldquo;dependent viscera sign&rdquo; (herniated organs layering against the posterior ribs), and the &ldquo;collar sign&rdquo; (narrowing of herniated organs and/or fat at the diaphragmatic defect).<sup>1-3</sup></p>
<p>Diaphragmatic rupture has the potential to be overlooked at initial evaluation due to small size and/or obscuration from adjacent pleural and parenchymal changes. Additionally, more immediately life-threatening traumatic injuries may capture the attention of the radiologist and the clinicians. Diaphragmatic defects typically require surgical intervention.<sup>1,2</sup> The herniated viscera are potentially at risk for complications if left untreated including obstruction, strangulation, and ischemia.<sup>1,2</sup></p>
<h3>Bochdalek Diaphragmatic Hernia</h3>
<p>Bochdalek hernia is a congenital diaphragmatic defect located posteriorly between the diaphragmatic pars lumbaris and pars costalis.<sup>1,2</sup> It is the most common congenital diaphragmatic hernia in adults and is usually discovered incidentally on cross-sectional imaging.<sup>1,2</sup> Bochdalek hernias usually contain fat, but abdominal viscera such as the kidney may also herniate through the defect.<sup>1,2</sup> Controversially, they are more common on the left.<sup>1,2</sup> They may be suggested by radiography, but can be occult. A common CT appearance is discontinuity of the posterior diaphragm with intrathoracic peritoneal fat herniation.<sup>1,2</sup></p>
<h3>Morgagni Diaphragmatic Hernia</h3>
<p>Morgagni hernia is a rare congenital diaphragmatic defect located anteriorly in the cardiophrenic space between the diaphragmatic pars costalis and pars sternalis.<sup>2</sup> They are much more common on the right.<sup>2</sup> Morgagni hernias may contain peritoneal fat, as well as abdominal solid organs and bowel. On plain films or CT, a Morgagni hernia will appear as a discontinuity of the diaphragm at the right cardiophrenic angle with intrathoracic peritoneal fat or solid organ herniation.<sup>2</sup></p>
<h3>Hiatal Hernia</h3>
<p>Hiatal hernias result from chronic widening at the esophageal hiatus due to weakening of the phrenicoesophageal membrane.<sup>2,4</sup> Prevalence increases with age. Hiatal hernias are generally categorized as sliding and paraesophageal, although mixed-type hiatal hernias also exist.<sup>2,4</sup> When the defect is severe, other abdominal viscera and/or fat can enter the thorax from a hiatal hernia.<sup>2,4 </sup>Hiatal hernias are typically evaluated on barium fluoroscopy examinations and can also be detected on radiographs. CT is not typically done for the detection of hiatal hernia, but they are often encountered incidentally on CT.</p>
<h2>Diagnosis</h2>
<p>Left traumatic diaphragmatic rupture with intrathoracic herniation of the stomach, spleen, and tail of the pancreas in the setting of major blunt chest trauma</p>
<h2>Summary</h2>
<p>This case of a left-sided diaphragmatic hernia had an initial wide differential considered. The key to narrowing the differential to the correct diagnosis of a traumatic diaphragmatic rupture is the location of the hernia, the CT evidence and history of trauma.</p>
<p>A Morgagni hernia would be found anteriorly and is very rarely found on the left side. A Bochdalek hernia would be located more posteriorly and typically contains fat. Although abdominal organs can enter a Bochdalek hernia, it would be extremely unusual to encounter a Bochdalek hernia containing the stomach, pancreatic tail, and spleen. Although a very large hiatal hernia can contain other abdominal organs, the defect should be able to be localized to the esophageal hiatus. The defect on this case was posterolateral in the left hemi-thorax, separate from the esophageal hiatus. Furthermore, such a large hiatal hernia would be highly unusual in a 27-year-old.</p>
<p>After applying these observations to the diagnostic considerations, a traumatic diaphragmatic rupture is the most appropriate diagnosis. This is an excellent example of a less common cause of a diaphragmatic hernia. As the treatment is surgical, it is important for the radiologist to be aware of this entity and to be able to differentiate it from other congenital and acquired diaphragmatic hernias that are much more frequently encountered.</p>
<h2>References</h2>
<ol>
<li>Desir A, Ghaye B. CT of blunt diaphragmatic rupture. Radiographics 2012;32(2):477-498.</li>
<li>Sandstrom CK, Stern EJ. Diaphragmatic hernias: a spectrum of radiographic appearances. Curr Probl Diagn Radiol 2011;40:95-115.</li>
<li>Kaewlai R, Avery LL, Asrani AV, et al. Multidetector CT of blunt thoracic trauma. Radiographics 2008;28(6):1555-1570.</li>
<li>Abbara S, Kalan MMH, Lewicki AM. Intrathoracic stomach revisited. Am J Roentgenol 2003 Aug;181(2):403-414.</li>
</ol>9786CT Imaging and Interventional Radiology in Solid Organ Injury2019-06-20T10:50:45-04:002019-06-20T10:50:45-04:00Jonathan A. Friedman, M.D., Thomas J.D. Wilczynski, D.O., Neelabh Maheshwari, M.D., Brian A. Bianco, D.O.<p>According to the World Health Organization, traumatic injuries kill more than 5 million people worldwide every year, accounting for 9% of the world&rsquo;s annual death toll. Approximately one-quarter of the 5 million deaths are the result of suicide (16%) and homicide (10%) with another one-quarter due to road traffic injuries.<sup>1</sup> Even larger is the burden of the tens of millions of nonlethal injuries resulting in hospitalizations, emergency department visits, and outpatient encounters.</p>
<p>The liver, spleen and kidneys are among the most commonly injured solid organs and are particularly vulnerable to blunt or penetrating trauma, including iatrogenic injury, leading to arterial laceration, parenchymal or peritoneal hemorrhage, subcapsular hematoma, pseudoaneurysm, or arteriovenous fistula formation.<sup>2</sup> In the emergent setting, focused assessment with sonography in trauma (FAST) is preferred over diagnostic peritoneal lavage as the screening tool for detecting intra-abdominal bleeding. Exploratory laparotomy is indicated in hemodynamically unstable patients, while hemodynamically stable patients typically undergo initial diagnostic imaging.</p>
<p>CT with intravenous contrast is the modality of choice because of its speed, availability, diagnostic accuracy, noninvasive nature, and ability to detect additional abdominal injuries that may require surgery.<sup>3</sup> Subsequent angiography may be necessary to evaluate for and potentially treat vascular injury. Typical angiographic findings in blunt abdominal trauma include contrast extravasation, subcapsular or parenchymal hematomas, and/or arterial occlusion, while penetrating trauma is usually more focal, demonstrating extravasation, pseudoaneurysms, and arteriovenous fistulas.<sup>2</sup></p>
<h2>Splenic Injury</h2>
<p>The spleen is among the most commonly injured organs in blunt abdominal trauma, accounting for up to 49% of all visceral injuries, with rates of injury in penetrating abdominal trauma less than that of other organs such as the liver and bowel.<sup>3,4</sup> A substantial portion of penetrating splenic injury arises from inadvertent intraoperative injury. In splenic trauma, the ability to preserve functional spleen is dwarfed by the need for prompt diagnosis and management. CT with intravenous contrast is the diagnostic gold standard for the assessment of hemodynamically stable patients with suspected splenic injury.<sup>2,3,5</sup></p>
<p>Imaging features of blunt splenic injury include laceration, nonperfusion, subcapsular or parenchymal hematoma, active hemorrhage, hemoperitoneum, sentinel clot and major vascular injury (<strong>Figures 1, 2</strong>). Laceration on CT appears as an irregular linear hypodensity. Subcapsular hematomas present as elliptical collections of hypodense blood between the capsule and enhanced parenchyma causing indentation or flattening of the organ contour (<strong>Figure 3</strong>). Ongoing bleeding appears as a punctate hyperdensity (85-350 HU) reflecting active contrast extravasation. Hemoperitoneum from splenic injury results in blood pooling in the left paracolic gutter and/or pelvis, possibly passing into the right upper quadrant.<sup>3</sup> A sentinel clot is typically a higher attenuation (45-80 HU) focus of clotted blood indicating an adjacent anatomic area of injury causing hemorrhage.<sup>6</sup></p>
<p>The most commonly used injury classification is the American Association for the Surgery of Trauma (AAST) grading scale, which demarcates 5 grades of splenic injury (grades I-V) with a higher number indicating worse severity.<sup>7</sup> The 2018 version reflects advancements of newer CT scanners and the relative success of nonoperative management (NOM). Notably is the addition of vascular injury on imaging as an indicator of high-grade injury. This includes pseudoaneurysm and arteriovenous fistula.</p>
<p>The utility of repeat CT imaging in the acute inpatient setting is controversial. In a study by Davis et al with 524 patients, NOM failure was most likely to occur within the first 72 hours following traumatic injury.<sup>8</sup> Their protocol of repeat CT with intravenous contrast at 48-72 hours after initial imaging found that 74% of splenic pseudoaneurysms were not present on initial imaging. Subsequent angioembolization lowered the overall failure rate for NOM to 6%. However, a study by Haan et al with 472 patients and a similar protocol found only 2 cases of delayed vascular injury on follow-up CT imaging, of which both were preceded by a drop in hematocrit.<sup>9</sup> The average AAST injury grade in this study was 1.8, which may indicate that repeat CT imaging may not be necessary for low-grade splenic injuries.</p>
<p>The use of angiographic embolization varies by institution with no accepted practice guidelines or consensus on patient selection criteria.<sup>5,10</sup> Some institutions favor aggressive endovascular management by performing embolization as the predominant therapy for grade III-V injuries and reserve surgery for patients with hemodynamic instability or peritonitis. Other institutions favor medical or surgical management as the first-line therapy and reserve endovascular techniques for active extravasation. Factors associated with NOM failure include age (&gt; 55), high-grade injury (&gt; grade III), active extravasation, large-volume hemoperitoneum, concomitant solid organ injury and vascular abnormalities.<sup>5</sup></p>
<p>Most authors support the recommendation of splenic surgery or angioembolization for grade IV and higher injuries, meaning any injury with evidence of a vascular component such as active hemorrhage or pseudoaneurysm.<sup>10</sup> According to Martin et al, &ldquo;literature supports practice paradigms with aggressive IR intervention in grades IV-V injuries and injuries with evidence of active arterial injury.&rdquo;<sup>11</sup> The Eastern Association for the Surgery of Trauma (EAST) recommends consideration of angiography for patients with AAST splenic injury grade III or higher, the presence of a contrast blush, moderate hemoperitoneum, or evidence of ongoing splenic bleeding.<sup>12</sup></p>
<p>Three common interventional radiology techniques used in the trauma setting include: transarterial embolization (TAE), balloon occlusion, and stent grafts.<sup>13</sup> Splenic arterial embolization (SAE) has proven successful with 3 general methods: proximal embolization, distal embolization, or a combination of both (<strong>Figure 4</strong>). Proximal embolization entails deploying coils or plugs approximately 2 cm distal to the dorsal pancreatic artery and is typically performed for diffuse splenic trauma (eg, shattered spleens and/or multiple areas of contrast extravasation) allowing collateral circulation from pancreatic, gastroduodenal, and gastric branches to maintain distal parenchymal perfusion (<strong>Figure 5</strong>). Distal embolization may be performed with Gelfoam (Pfizer Inc., New York, NY) distributed by flow or superselective embolization of a focal defect or single injured vessel with coils or particles, with the latter technique requiring increased time and technical skill (<strong>Figure 6</strong>).<sup>13,14</sup></p>
<p>Splenic artery embolization carries a high success rate. A systematic review and meta-analysis performed by Rong et al of 876 patients with 2 study sets demonstrated a primary success rate of SAE to be 90% with an overall incidence of severe complications at 20% and cases requiring further surgical intervention even fewer at 6%.<sup>15</sup> Although success rates were higher for proximal embolization, no statistically significant differences between success rates and embolization location were identified, although the study suggested a reduced risk of adverse events with proximal SAE compared to distal and combination embolization. The use of coils is associated with higher success rates and a lower risk of developing life-threatening complications compared to Gelfoam.<sup>15</sup></p>
<h2>Hepatic Injury</h2>
<p>Similar to splenic trauma, hemodynamic status and contrast CT imaging are the cornerstones in directing management by assessing the liver parenchyma as well as evaluating for other signs of injury including hemoperitoneum, pneumoperitoneum, hepatic venous injury, periportal low attenuation, sentinel clot(s), additional organ injuries, and active bleeding (<strong>Figure 7, 8</strong>).<sup>16</sup> Active hemorrhage is identified by a contrast blush, seen as a hyperattenuating focus on arterial or venous phase imaging and has a similar Hounsfield unit with nearby arterial vasculature.<sup>16</sup> If there is uncertainty as to whether the hyperattenuating focus represents active hemorrhage, delayed images may show worsening contrast extravasation or morphologic changes.</p>
<p>Follow-up CT with intravenous contrast may play a role in management. Re-evaluation using CT is recommended when there is a persistent systemic inflammatory response syndrome (SIRS), increasing or persistent abdominal pain, jaundice, or a decrease in hemoglobin. Even in asymptomatic patients repeat CT may be useful. A study involving 259 patients with blunt liver trauma reimaged patients 4-5 days following traumatic injury and found that 3% of asymptomatic patients had developed a pseudoaneurysm.<sup>17</sup> In a study by Yoon et al, the authors explained that CT is useful in the assessment of delayed complications of blunt liver trauma, including hemorrhage, hepatic or perihepatic abscess; post-traumatic pseudoaneurysm; hemobilia; and biliary complications such as biloma and bile peritonitis.<sup>18</sup> Their study also confirmed that follow-up CT is needed for patients with high-grade liver injuries to mitigate future issues requiring intervention.</p>
<p>The AAST scale for liver injury demarcates 5 grades of splenic injury (grades I-V) with a higher number indicating worse severity.<sup>7</sup> Hepatic trauma can be divided into 3 management classifications: NOM, TAE, and surgery. CT can accurately characterize the severity of hepatic injury and has reduced the number of patients undergoing surgery. According to EAST, &ldquo;NOM of blunt hepatic injuries currently is the treatment modality of choice in hemodynamically stable patients, irrespective of the grade of injury or patient age,&rdquo; but only in an environment that can support monitoring for acute decompensation and provide emergent interventional or surgical management.<sup>19</sup> Patients with hemodynamic instability or peritonitis still require surgical intervention as the first-line option; however, TAE may be considered before surgery if the patient transiently responds to resuscitative efforts and imaging shows identifiable arterial bleeding.</p>
<p>Even in high-grade injuries, the use of NOM in hemodynamically stable patients remains successful. A meta-analysis conducted by Melloul et al utilized data from 4743 patients with grade III-V hepatic injury. NOM in hemodynamically stable patients with grade III-V hepatic injury showed a success rate of 82% to 100%, an overall 90-day mortality rate of 0% to 8%, and liver-related mortality of 0% to 4%. Similarly, TAE showed a success rate of 81% to 100%, with biliary leak cited as the most common complication (5.9%).<sup>20</sup> TAE should be utilized after the identification of contrast blush on CT imaging. A retrospective series with 351 blunt hepatic trauma patients identified high-grade injury (grade III-V) and CT angiographic contrast blush as prognostic indicators for the likelihood of NOM failure.<sup>21</sup> In those patients, TAE in NOM can reduce the likelihood of failure and the need for surgery (<strong>Figure 9</strong>).</p>
<p>TAE can also be used if clinical signs indicate continuing or worsening hemorrhage in the setting of known hepatic injury. Celiac and mesenteric arteriography localizes previously seen or clinically suspected active hemorrhage. Even without a blush on CT, angiography and TAE may be performed if a patient shows clinical signs of hemorrhage. One study identified all liver trauma patients with severe liver injuries from their institution over 10 years, regardless of hemodynamic status, and all underwent TAE with a success rate of 90%.<sup>22</sup></p>
<p>Hepatic TAE is successful and generally well tolerated by patients with procedure-related death being extremely rare.<sup>23</sup> A systematic review by Virdis et al evaluated 3855 patients and found success rates of TAE to range between 80% to 97%.<sup>24</sup> All-cause mortality following TAE is &lt; 10%; the risk of liver-related mortality is rated at 6%; and the most significant possible risks of TAE include bile leak at 5.7%, hepatic necrosis, and abscess.<sup>24</sup> Other risks include gallbladder infarct if the right hepatic artery is embolized without careful attention to the cystic artery.<sup>24,25</sup> Most TAE complications can be treated with NOM or endovascular approaches, such as percutaneous drainage, cholangiography or endoscopic retrograde cholangiopancreatography.<sup>24,25</sup></p>
<p>Biliary and hepatic venous injury can also be repaired by interventional radiology. Hepatic venous trauma is almost always handled surgically, but there are cases of endovascular repair in which 2 endovascular covered stents were successfully placed to bridge flow from the hepatic vein to the IVC following traumatic injury.<sup>25</sup> Biliary injuries may develop into a complicating biloma, abscess, stricture, or arteriobiliary fistula, all of which are amenable to repair through percutaneous transhepatic cholangiography, stenting, embolization, and/or drain placement.<sup>26,27</sup></p>
<h2>Renal Injury</h2>
<p>The kidneys are the third most common abdominal organ to be traumatically injured. Blunt trauma is a major mechanism, but there is an increasing number of iatrogenic causes (both during interventional and intraoperative procedures) due to the rise in interventional procedures such as renal artery angioplasty, stenting, percutaneous biopsy, nephrostomy, and nephro-ureterolithotomy (<strong>Figures 10-12</strong>).<sup>28</sup></p>
<p>Traumatic renal injuries are identified on CT imaging with intravenous contrast and graded using the AAST classification system (grade I-V, with grade V the most severe), which takes into account specific complications such as renal vascular thrombosis, segmental renal artery or vein injury, and damage to the collecting system.<sup>7</sup> There has been a trend toward the NOM of renal traumatic injury that is often institution-dependent and based on the injury grade and the patient&rsquo;s clinical status. Grade I-III parenchymal or vascular injuries are always initially managed conservatively with observation.<sup>29</sup> NOM is also increasingly becoming the standard of care for grades IV and V parenchymal injury provided the patient is hemodynamically stable and there is no evidence of active contrast extravasation or urine leakage. A multicenter study of 206 patients with grade IV or V blunt renal injury demonstrated safe NOM of hemodynamically stable patients, with a nonoperative failure rate of 7.8%.<sup>30</sup> Furthermore, NOM decreases ICU stay, lowers transfusion requirements, and yields fewer complications.<sup>31</sup> Current guidelines from the American Urological Society recommend observation in hemodynamically stable patients and intervention in hemodynamically unstable patients.<sup>32</sup></p>
<p>Surgical treatment is always indicated for hemodynamically unstable patients, in grade V vascular injury (avulsion of the renal artery, vein, or collecting system), and in expanding retroperitoneal hematomas discovered during exploratory laparotomy for other abdominal injury. Ureteral stenting is the treatment of choice in lacerations involving the collecting system and ureteropelvic junction laceration.<sup>29</sup></p>
<p>Several retrospective studies have shown early follow-up CT imaging does not detect or prevent any urologic complications. For example, a study at the University of Tennessee of 207 patients who sustained grade I-III renal injury found that follow-up CT with intravenous contrast in renal cortical and excretory phases did not detect or prevent any urologic complications.<sup>33</sup> Another study at Cork University Hospital of 102 patients with grade I-V renal injury demonstrated all complications of renal trauma were symptomatic.<sup>34</sup> The European Association of Urology Guidelines refer to repeat imaging for renal injuries and recommend repeat CT imaging in grades I-IV only if the patient demonstrates clinical deterioration such as fever, flank pain, and decreasing hemoglobin.<sup>35</sup></p>
<p>Interventional radiology is slowly taking a larger role in the treatment of blunt renal trauma with selective renal artery embolization (<strong>Figure 13</strong>); however, there is little data reported in the literature.<sup>29</sup> A study of 20 patients who underwent renal artery embolization for blunt trauma and gross hematuria demonstrated successful cessation of bleeding in all patients.<sup>36</sup> A study of 52 patients with grade III or IV renal laceration showed peri-renal hematoma size and contrast extravasation to be predictors for renal artery embolization.<sup>37</sup> Renal pseudoaneurysm is another possible vascular injury from blunt renal trauma. Again, data are limited to case series, including a study of 5 patients treated successfully with embolization.<sup>38</sup></p>
<h2>Conclusion</h2>
<p>Identification and management of abdominal organ injury is rapidly evolving. Injuries once identified and treated operatively are now diagnosed by CT and predominantly treated nonoperatively and/or via interventional techniques in hemodynamically stable patients. These more conservative and minimally invasive techniques are driven by the goals of increased patient safety and reduced morbidity and mortality. Given these trends, there will likely be an increasing role for interventional radiology in patient management and treatment as part of a multidisciplinary clinical team.</p>
<h2>References</h2>
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<li>Hassan R, Abd Aziz A, Md Ralib AR, Saat A. Computed tomography of blunt spleen injury: a pictorial review. Malays J Med Sci 2011;18(1):60-67.</li>
<li>Joseph B, Khalil M, Rhee P. Penetrating injuries to the spleen and kidney: an evolution in progress. Curr Trauma Reports 2015;1(2):76-84. doi:10.1007/s40719-015-0016-9.</li>
<li>Zarzaur BL, Rozycki GS. An update on nonoperative management of the spleen in adults. Trauma Surg Acute Care Open. 2017;2(1):e000075. doi:10.1136/tsaco-2017-000075.</li>
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<li>Davis KA, Fabian TC, Croce MA, et al. Improved success in nonoperative management of blunt splenic injuries: embolization of splenic artery pseudoaneurysms. J Trauma 1998;44(6):1008-1013; discussion 1013-5. http://www.ncbi.nlm.nih.gov/pubmed/9637156. Accessed April 10, 2019.</li>
<li>Haan JM, Boswell S, Stein D, Scalea TM. Follow-up abdominal CT is not necessary in low-grade splenic injury. Am Surg 2007;73(1):13-18. http://www.ncbi.nlm.nih.gov/pubmed/17249449. Accessed April 10, 2019.</li>
<li>Saksobhavivat N, Shanmuganathan K, Chen HH, et al. Blunt splenic injury: use of a multidetector CT-based splenic injury grading system and clinical parameters for triage of patients at admission. Radiology 2015;274(3):702-711. doi:10.1148/radiol.14141060.</li>
<li>Martin JG, Shah J, Robinson C, Dariushnia S. Evaluation and management of blunt solid organ trauma. Tech Vasc Interv Radiol 2017;20(4):230-236. doi:10.1053/j.tvir.2017.10.001.</li>
<li>Stassen NA, Bhullar I, Cheng JD, et al. Selective nonoperative management of blunt splenic injury: an Eastern Association for the Surgery of Trauma practice management guideline. J Trauma Acute Care Surg 2012;73(5 Suppl 4):S294-300. doi:10.1097/TA.0b013e3182702afc.</li>
<li>Gould JE, Vedantham S. The role of interventional radiology in trauma. Semin Intervent Radiol 2006;23(3):270-278. doi:10.1055/s-2006-948766.</li>
<li>Lopera JE. Embolization in trauma: principles and techniques. Semin Intervent Radiol 2010;27(1):14-28. doi:10.1055/s-0030-1247885.</li>
<li>Rong J-J, Liu D, Liang M, et al. The impacts of different embolization techniques on splenic artery embolization for blunt splenic injury: a systematic review and meta-analysis. Mil Med Res 2017;4:17. doi:10.1186/s40779-017-0125-6.</li>
<li>Soto JA, Anderson SW. Multidetector CT of blunt abdominal trauma. Radiology 2012;265(3):678-693. doi:10.1148/radiol. 12120354.</li>
<li>&Oslash;sterballe L, Helgstrand F, Axelsen T, Hillings&oslash; J, Svendsen LB. Hepatic pseudoaneurysm after traumatic liver injury: is CT follow-up warranted? J Trauma Manag Outcomes 2014;8:18. doi:10.1186/1752-2897-8-18.</li>
<li>Yoon W, Jeong YY, Kim JK, et al. CT in blunt liver trauma. Radiographics 2005;25(1):87-104. doi:10.1148/rg.251045079.</li>
<li>Stassen NA, Bhullar I, Cheng JD, et al. Nonoperative management of blunt hepatic injury: an Eastern Association for the Surgery of Trauma practice management guideline. J Trauma Acute Care Surg 2012;73(5 Suppl 4):S288-93. doi:10.1097/TA.0b013e318270160d.</li>
<li>Melloul E, Denys A, Demartines N. Management of severe blunt hepatic injury in the era of computed tomography and transarterial embolization: a systematic review and critical appraisal of the literature. J Trauma Acute Care Surg 2015;79(3):468-474. doi:10.1097/TA.0000000000000724.</li>
<li>Xu H, Jie L, Kejian S, et al. Selective angiographic embolization of blunt hepatic trauma reduces failure rate of nonoperative therapy and incidence of post-traumatic complications. Med Sci Monit 2017;23:5522-5533.</li>
<li>Inukai K, Uehara S, Furuta Y, Miura M. Nonoperative management of blunt liver injury in hemodynamically stable versus unstable patients: a retrospective study. Emerg Radiol 2018;25(6):647-652. doi:10.1007/s10140-018-1627-6.</li>
<li>Green CS, Bulger EM, Kwan SW. Outcomes and complications of angioembolization for hepatic trauma: A systematic review of the literature. <em>J Trauma Acute Care Surg</em> 2016;80(3):529-537. doi:10.1097/TA.0000000000000942.</li>
<li>Virdis F, Reccia I, Di Saverio S, et al. Clinical outcomes of primary arterial embolization in severe hepatic trauma: A systematic review. Diagn Interv Imaging 2019;100(2):65-75. doi:10.1016/j.diii.2018.10.004.</li>
<li>Jeph S, Ahmed S, Bhatt RD, Nadal LL, Bhanushali A. Novel use of interventional radiology in trauma. J Emerg Crit Care Med 2017;1(12):40-40. doi:10.21037/jeccm.2017.10.04.</li>
<li>Thompson CM, Saad NE, Quazi RR, Darcy MD, Picus DD, Menias CO. Management of iatrogenic bile duct injuries: role of the interventional radiologist. RadioGraphics 2013;33(1):117-134. doi:10.1148/rg.331125044.</li>
<li>Stefaczyk L, Polguj M, Szubert W, Chrząstek J, Jurałowicz P, Garcarek J. Arterio-biliary fistulas: What to choose as endovascular treatment? Vascular 2018;26(4): 445-448. doi:10.1177/1708538117743178.</li>
<li>Loffroy R, Chevallier O, Gehin S, et al. Endovascular management of arterial injuries after blunt or iatrogenic renal trauma. Quant Imaging Med Surg 2017;7(4):434-442. doi:10.21037/qims.2017.08.04.</li>
<li>Bonatti M, Lombardo F, Vezzali N, et al. MDCT of blunt renal trauma: imaging findings and therapeutic implications. Insights Imaging 2015;6(2):261-272. doi:10.1007/s13244-015-0385-1.</li>
<li>van der Wilden GM, Velmahos GC, Joseph DK, et al. Successful nonoperative management of the most severe blunt renal injuries: a multicenter study of the research consortium of New England Centers for Trauma. JAMA Surg 2013;148(10):924-931. doi:10.1001/jamasurg.2013.2747.</li>
<li>Altman AL, Haas C, Dinchman KH, Spirnak JP. Selective nonoperative management of blunt grade 5 renal injury. J Urol 2000;164(1):21-27..</li>
<li>Morey AF, Brandes S, Dugi DD 3rd, et al. Urotrauma: AUA guideline. J Urol 2014;192(2):327-335. doi:10.1016/j.juro.2014.05.004.</li>
<li>Malcolm JB, Derweesh IH, Mehrazin R, et al. Nonoperative management of blunt renal trauma: is routine early follow-up imaging necessary? BMC Urol 2008;8:11. doi:10.1186/1471-2490-8-11.</li>
<li>Breen KJ, Sweeney P, Nicholson PJ, Kiely EA, O&rsquo;Brien MF. Adult blunt renal trauma: routine follow-up imaging is excessive. Urology 2014;84(1):62-67. doi:10.1016/j.urology.2014.03.013.</li>
<li>Summerton DJ, Djakovic N, Kitrey ND, et al. Guidelines on Urological Trauma; 2014. https://uroweb.org/wp-content/uploads/24-Urological-Trauma_LR.pdf. Accessed February 21, 2019.</li>
<li>Vozianov S, Sabadash M, Shulyak A. Experience of renal artery embolization in patients with blunt kidney trauma. Cent Eur J Urol 2015;68(4):471-477. doi:10.5173/ceju.2015.491.</li>
<li>Nuss GR, Morey AF, Jenkins AC, et al. Radiographic predictors of need for angiographic embolization after traumatic renal injury. J Trauma 2009;67(3):578-82; discussion 582. doi:10.1097/TA.0b013e3181af6ef4.</li>
<li>Poulakis V, Ferakis N, Becht E, Deliveliotis C, Duex M. Treatment of renal-vascular injury by transcatheter embolization: immediate and long-term effects on renal function. J Endourol 2006;20(6):405-409. doi:10.1089/end.2006.20.405.</li>
</ol>9784Imaging of Traumatic Intracranial Hemorrhage2019-06-20T09:09:32-04:002019-06-20T09:09:32-04:00Christian Koegel, M.D., Raluca McCallum, M.D., Mark Greenhill, B.S., Diana López García, M.D., Ajay Kohli, M.D., Mea Mallon, M.D<p>Intracranial hemorrhage (ICH) is a common entity encountered in clinical emergency medicine. Imaging is the cornerstone in the diagnosis of traumatic ICH. In a large study of patients with a head injury and a decreased Glasgow Coma Scale (GCS), 46% of patients demonstrated intracranial hemorrhage. Of these, 30% were subdural hematomas (SDH), 22% were epidural hematomas (EDH), 22% were intraparenchymal hemorrhages (IPH), and 14% were subarachnoid hemorrhages (SAH).<sup>1</sup> Current literature reports up to 72% incidence of diffuse axonal injury (DAI) in moderate to severe head injury.<sup>2</sup> Timely and accurate diagnoses of ICH is key to successful patient management given the emergent nature of ICH.</p>
<p>CT is the initial modality of choice due to its accuracy, short study time, low cost, and robustness against artifacts. MR is also used given its increased sensitivity in detecting DAI, as well as subacute and chronic hemorrhage.<sup>3</sup> Although lumbar punctures were previously more common in the diagnostic workup of SAH, there has been a paradigm shift away from performing this procedure, as nonenhanced CT (NECT) has been shown to be highly accurate in detecting SAH when performed within 6 hours of symptom onset.<sup>4</sup></p>
<p>This article will review the key vascular anatomy associated with ICH followed by a strategy for imaging evaluation and reporting. This is followed by a detailed review of the different types of traumatic ICH with an emphasis on imaging findings.</p>
<h2>Meningeal Vascular Anatomy</h2>
<p>The three meningeal layers (dura, arachnoid and pia mater) are perfused by the anterior, middle and posterior meningeal arteries. The anterior and posterior meningeal arteries originate from the anterior ethmoidal and ascending pharyngeal arteries, respectively, and perfuse dura of the anterior and posterior cranial fossa.<sup>5</sup> The middle meningeal artery, a maxillary artery branch, enters the skull at the foramen spinosum.<sup>5</sup> Trauma to the parietotemporal skull can lacerate these vessels resulting in hemorrhage.<sup>6</sup></p>
<p>The meningeal venous drainage occurs via dural sinuses, located between the periosteum of the skull and the dura mater, mainly via the superior sagittal, transverse and sigmoid sinuses. Central brain regions drain via the inferior sagittal sinus and great vein of Galen into the straight sinus. Relatively small venous blood volumes exit the skull through the cavernous sinus and ophthalmic veins.<sup>7</sup> Injury to bridging veins leads to SDH; injury to the cerebral veins/arteries leads to SAH. Skull-base fractures can injure a dural sinus, which bears the probability of massive blood loss into an extra-axial hematoma.</p>
<h2>Imaging Evaluation and Reporting</h2>
<p>Given the critical nature of ICH, the interpreting physician must take necessary steps to prevent overlooking ICH on imaging. Although axial imaging is the standard for evaluating head CT, using additional reconstructions should be considered in routine clinical practice. ICH detection rate increases when axial and coronal images are viewed.<sup>9</sup> Among missed acute intracranial hemorrhages, SDH accounts for 39%, followed by SAH with 33%.<sup>10</sup> A customized checklist approach (<strong>Table 1</strong>) may be beneficial to the radiologist, particularly to ensure classic areas for subtle findings are evaluated (<strong>Figure 1</strong>). CT windows should also be considered when interpreting studies as subtle findings may be obscured due to windowing. In addition to standard CT head windows, the authors&rsquo; institution has found a width of 99 Hounsfield units, level of 93 HU images can make hemorrhage optically more conspicuous (<strong>Figure 2</strong>).</p>
<p>Additionally, it is important to have a general understanding of imaging findings and information that referring physicians need to guide management. In particular, findings that help determine a need for surgical decompression/evacuation should be reported, although the decision for surgery is based on clinical information in addition to imaging. When encountering ICH on CT or MR several items should be routinely reported including midline shift (particularly if &gt; 5 mm), hematoma thickness/volume, mass effect, effacement of ventricles and/or cisterns, evidence of herniation, evidence of hydrocephalus, and coexistent injuries such as skull fractures and intracranial foreign bodies.<sup>11</sup></p>
<h2>Imaging Features of Intracranial Hemorrhage</h2>
<h3>Diffuse Axonal Injury</h3>
<p>Unequal rotational and acceleration-deceleration forces cause the brain to pivot around the brainstem, causing stretching and shearing of axons and resulting in the clinical diagnosis of DAI. Shear forces peak at the grey-white matter interface, due to its peripheral location and differences in tissue density; hence, 67% of DAI lesions are in this region.<sup>12</sup> In more severe cases, additional sites of injury occur in the brainstem. Within hours, axonal deformation damages its cytoskeleton, resulting in arrest of axoplasmic flow on a microscopic level, followed by axonal swelling and subsequently axon rupture.<sup>13</sup> Mechanisms of injury vary, but include high-impact falls and motor vehicle accidents.</p>
<p>Foci of axonal edema with or without hemorrhage are imaging findings of DAI and these foci may vary in size (<strong>Figure 3</strong>). Despite DAI being present in up to 72% of patients with moderate to severe head injuries, 50% to 80% of initial CT and MRI studies are negative.<sup>2</sup> MRI is more sensitive than CT in detecting lesions (<strong>Figure 4</strong>).<sup>12-14</sup> Gradient echo (GRE) and susceptibility-weighted imaging (SWI) are the most sensitive sequence, revealing the highest number of lesions at the highest number of locations compared to other MR sequences. The classic triad seen in DAI is diffuse damage to axons, a focal lesion in the corpus callosum, and a focal lesion in the dorsolateral quadrant of the rostral brainstem adjacent to the superior cerebellar peduncles.<sup>12</sup> DAI lesions detected within 4 weeks after injury improve functional status and long-term outcome due to changes in patient management.<sup>15</sup> Therefore, MRI is recommended within 4 weeks of traumatic brain injury (TBI).<sup>16</sup></p>
<h2>Intraparenchymal Hemorrhage</h2>
<p>Traumatic acute IPH, commonly referred to as a cerebral contusion, usually occurs after a significant direct head injury. It commonly involves brain parenchyma adjacent to bony protuberance/dural fold.<sup>5</sup> CT displays a patchy, irregular, hyperdense area of acute hemorrhage on an edematous background (<strong>Figure 5</strong>). Hemorrhages may be multiple and bilateral. Cerebral edema may be relatively mild acutely; however, progression of cerebral edema is common and can result in midline shift and herniation syndromes. IPH can be complicated by continued enlargement and/or re-hemorrhage. Likewise, new lesions can be detected on follow-up imaging. MRI is useful to identify traumatic intraparenchymal damage without blood products, termed nonhemorrhagic cerebral contusion (<strong>Figure 6</strong>). Sequelae after resolution are common and include gliosis, encephalomalacia and associated volume loss.</p>
<h3>Subdural Hematoma</h3>
<p>Acute SDH is characterized by an extra-axial crescent-shaped hemorrhage in a potential space between the dura and arachnoid. A direct blow to the head is not necessary to incur an SDH. Instead, an SDH may be related to acceleration-deceleration forces secondary to the impact from a fall or shaking of an infant.<sup>17</sup> Regardless of the mechanism, shear forces on the bridging veins or cortical arteries can lead to injury and rupture.<sup>18-20</sup> Elderly are predisposed to develop SDH due to cortical atrophy. Additionally, anticoagulants and antiplatelet agents (<strong>Figure 7</strong>) raise concern for increased risk of hemorrhage. Contrary to epidural hematomas, classic SDH are limited by dural duplications, but can cross suture lines and, therefore, can extend over an entire hemisphere. The vast majority of small, atypically shaped, extra-axial hemorrhages are due to a low-pressure venous injury causing an SDH with continued CT follow-up suggested if clinical doubt remains as to whether an extra-axial blood collection reflects an EDH or SDH.</p>
<p>It is valuable for the radiologist to be generally aware of the appearance of blood products on CT based on the acuity. Although imaging may not occur this early, in the first few hours (hyperacute phase), SDH might be isodense to the underlying cortex, as it is still liquid (40-50 HU), and may not be detectable. Hemorrhage becomes increasingly dense as it coagulates and condenses during the acute phase (0-3 days) due to clot retraction by a decreased fluid component and relative increase in iron content in the red blood cells. Those clots measure between 80-100 HU and show the typical hyperattenuation. The attenuation decreases in the subacute phase as the blood products degrade and eventually becomes similar to CSF density in the chronic phase (<strong>Figure 8</strong>).<sup>21 </sup></p>
<p>SDH requires heightened vigilance and follow-up imaging to ensure early detection of complications, such as continued bleeding, rebleeding (8% of cases), midline shift, or herniation.<sup>22</sup> Mixed attenuation blood in which isodense areas are intermixed by hyperdense areas suggest active (re)bleeding, which is termed the &ldquo;swirl sign&rdquo; on NECT. Cerebral spinal fluid in the subdural space (subdural hygromas) is thought to be related to subdural hematomas. An arachnoid membrane tear with a &ldquo;flap-valve&rdquo; mechanism results in CSF leakage into the subdural space.<sup>23,24</sup></p>
<h3>Epidural Hematoma</h3>
<p>Hemorrhage into a potential space between the inner table of the skull and the dura mater occurs in 1% of minor head injury and 10% following head injury in patients who present in a comatose state.<sup>25,26</sup> A provided history of head injury days-to-months prior to imaging should not eradicate the possibility of an EDH, as 20% to 50% of patients experience a symptom-free lucid interval.<sup>27</sup> Of patients with an EDH, 91% suffer from an associated skull fracture.<sup>28</sup> Typically supratentorially located, EDH frequently involves injury to the middle meningeal artery or anterior ethmoidal artery. Rapid hematoma expansion is common due to the relatively high pressure of arterial blood.<sup>29 </sup>Classic CT findings are a high-density convex or biconvex shaped extra-axial fluid collection that does not cross the sutures (<strong>Figure 9</strong>).</p>
<p>Venous epidural hemorrhage accounts for 5% to 10% of all EDH and occurs at specific locations including the vertex (superior sagittal sinus injury), anterior middle cranial fossa (sphenoparietal sinus injury), and posterior occipital region (transverse/sigmoid sinus injury). The latter can rapidly cause tonsillar herniation. However, the majority of venous EDH are unlikely to expand because venous pressure is insufficient to further strip off the dura from the skull.<sup>30</sup> Similar to arterial EDH, an associated fracture/diastasis is common. Venous EDH typically displaces the sinus away from the fracture and, in contrast to arterial EDH, can occasionally cross suture lines (<strong>Figure 10</strong>). One should suspect a venous EDH if a skull fracture runs through the expected location of a dural sinus.</p>
<p>Rarely, direct bleeding from a skull fracture causes EDH.<sup>5</sup> Similar to the other causes of ICH, co-existent and/or complicating findings may be encountered including mass effect, rebleeding, herniation, brain edema, and/or intraparenchymal hemorrhage.<sup>31-32</sup> Similar to SDH, the appearance of the blood on CT and MR depends on its age, as hemoglobin is progressively degraded over time.<sup>33</sup></p>
<h2>Traumatic Subarachnoid Hemorrhage</h2>
<p>Traumatic SAH (tSAH) results from disruption of pial vessels with bleeding into the subarachnoid space. It is often coexistent with other pathologies in the setting of trauma. Vessel injury more commonly arises in the cerebral convexities/sulci following a high-impact mechanical force to the head. Of patients with severe TBI, 40% develop tSAH.<sup>34</sup> Be cautious with SAH in the setting of acute trauma as differential diagnosis includes tSAH as well as nontraumatic SAH (eg, ruptured aneurysm) that may have preceded (and perhaps led to) the reported trauma (<strong>Figure 11</strong>). Differentiating traumatic from nontraumatic SAH by imaging is not always possible. However, SAH identified around the cerebral convexities with relative sparing of the basilar cisterns around the circle of Willis would favor trauma.<sup>35</sup> Similarly, SAH associated with other signs of trauma on CT such as a countercoup pattern associated with a parenchymal contusion may also favor a traumatic etiology. When doubt exists, the CT or traditional angiography may be performed for further evaluation to exclude an aneurysm.</p>
<p>Imaging characteristics that portend a worse prognosis include other evidence of brain trauma including brain contusions, especially if enlarging.<sup>36</sup> Complications of tSAH include hydrocephalus and cerebral vasospasm.<sup>35,37</sup> <strong>Table 2</strong> summarizes differentiating key features of EDH, SDH and SAH.</p>
<h2>Conclusion</h2>
<p>Traumatic intracranial hemorrhage is an urgent finding requiring prompt and accurate evaluation by the interpreting radiologist with excellent communication and documentation of key findings that may affect patient management. Given the trauma and further complicating patient management, additional critical coexistent injuries may also be present and require urgent treatment. Thus, at many medical centers a multidisciplinary neurotrauma team guides management and determines the need for surgical decompression/evacuation (<strong>Figure 12</strong>).</p>
<p>Furthermore, the radiologist must be vigilant about new and/or worsening edema, midline shift, signs of hydrocephalus, worsening hemorrhage (rebleeding), or other complicating factors on follow-up studies that may alter patient management. Medical and surgical management in these patients is complex and multifactorial requiring timely and accurate imaging information, thus solidifying the radiologists&rsquo; key role in the management of traumatic ICH.</p>
<h2>References</h2>
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<li>Kidwell CS, Chalela JA, Saver JL, et al. Comparison of MRI and CT for detection of acute intracerebral hemorrhage. JAMA 2004;292(15):1823-1830.</li>
<li>Carpenter CR, Hussain AM, Ward MJ, et al. Spontaneous subarachnoid hemorrhage: a systematic review and meta-analysis describing the diagnostic accuracy of history, physical examination, imaging, and lumbar puncture with an exploration of test thresholds. Acad Emerg Med 2016;23(9):963-1003.</li>
<li>Yousem, D, Zimmerman R, Grossman R. In Nadgir R, ed. Neuroradiology: The Requisites. 3rd Edition. Philadelphia, PA: Mosby/Elsevier. 2010. https://www.elsevier.com/books/neuroradiology-the-requisites/yousem/978-0-323-04521-6. Accessed April 14, 2019.</li>
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<li>Mancall EL, Brock, DG. Gray&rsquo;s Clinical Neuroanatomy. Philadelphia, PA: Elsevier/Saunders; 2011. https://www.us.elsevierhealth.com/grays-clinical-neuroanatomy-9781416047056.html. Accessed April 14, 2019.</li>
<li>Cranial Vault &amp; Skull Base - Diagnosis - Skull base, Anterior skull base fractures - AO Surgery Reference. https://www2.aofoundation.org/wps/portal/!ut/p/a0/04_Sj9CPykssy0xPLMnMz0vMAfGjzOKN_A0M3D2DDbz9_UMMDRyDXQ3dw9wMDAzMjfULsh0VAbWjLW0!/?bone=CMF&amp;classification=93-Skull%20base%2C%20Anterior%20skull%20base%20fractures&amp;segment=Cranium&amp;showPage=diagnosis&amp;teaserTitle=&amp;contentUrl=srg/93/01-Diagnosis/skull_base-skull_base.jsp. Accessed April 14, 2019.</li>
<li>Wei SC, Ulmer S, Lev MH, Pomerantz SR, Gonz&aacute;lez RG, Henson JW. Value of coronal reformations in the CT evaluation of acute head trauma. Am J Neuroradiol 2010;31(2):334-339.</li>
<li>Strub WM, Leach JL, Tomsick T, Vagal A. Overnight preliminary head CT interpretations provided by residents: locations of misidentified intracranial hemorrhage. Am J Neuroradiol 2007;28(9)1679-1682. http://www.ajnr.org/content/28/9/1679. Accessed April 14, 2019.</li>
<li>Escobedo LVS, Habboushe J, Kaafarani H, Velmahos G, Shah K, Lee J. Traumatic brain injury: a case-based review. World J Emerg Med 2013;4(4):252-259.</li>
<li>Parizel PM, Ozsarlak, Van Goethem JW, et al. Imaging findings in diffuse axonal injury after closed head trauma. Eur Radiol. 1998;8(6):960-965.</li>
<li>Hill CS, Coleman MP, Menon DK. Traumatic axonal injury: mechanisms and translational opportunities. Trends Neurosci 2016;39(5):311-324.</li>
<li>Kinoshita T, Moritani T, Hiwatashi A, et al. Conspicuity of diffuse axonal injury lesions on diffusion-weighted MR imaging. Eur J Radiol 2005;56(1):5-11.</li>
<li>Bansal M, Sinha VD, Bansal J. Diagnostic and prognostic capability of newer magnetic resonance imaging brain sequences in diffuse axonal injury patient. Asian J Neurosurg 2018;13(2):348-356.</li>
<li>Moen KG, Brezova V, Skandsen T, H&aring;berg AK, Folvik M, Vik A. Traumatic axonal injury: the prognostic value of lesion load in corpus callosum, brain stem, and thalamus in different magnetic resonance imaging sequences. J Neurotrauma 2014;31(17):1486-1496.</li>
<li>Gennarelli TA, Thibault LE. Biomechanics of acute subdural hematoma. J Trauma 1982;22(8):680-686.</li>
<li>DeKosky ST, Ikonomovic MD, Gandy S. Traumatic brain injury--football, warfare, and long-term effects. N Engl J Med 2010;363(14):1293-1296.</li>
<li>Maxeiner H, Wolff M. Pure subdural hematomas: a postmortem analysis of their form and bleeding points. Neurosurgery 2007;61(1 Suppl):267-272; discussion 272-273.</li>
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<li>Berlin L. Avoiding errors in radiology: case-based analysis of causes and preventive strategies. JAMA 2011;306(11):1267-1268.</li>
<li>Lee K-S, Shim J-J, Yoon S-M, Doh J-W, Yun I-G, Bae H-G. Acute-on-Chronic subdural hematoma: not uncommon events. J Korean Neurosurg Soc 2011;50(6):512-516.</li>
<li>Duy L, Badeeb A, Duy W, et al. CT Attenuation of acute subdural hematomas in patients with anemia. J Neuroimaging 2019, February 16.</li>
<li>McCluney KW, Yeakley JW, Fenstermacher MJ, Baird SH, Bonmati CM. Subdural hygroma versus atrophy on MR brain scans: &ldquo;the cortical vein sign.&rdquo; AJNR Am J Neuroradiol 1992;13(5):1335-1339.</li>
<li>Baykaner K, Alp H, Ceviker N, Keskil S, Se&ccedil;kin Z. Observation of 95 patients with extradural hematoma and review of the literature. Surg Neurol 1988;30(5):339-341.</li>
<li>Freytag E. Autopsy findings in head injuries from blunt forces. Statistical evaluation of 1,367 cases. Arch Pathol 1963;75:402-413.</li>
<li>Kushner D. Mild traumatic brain injury: toward understanding manifestations and treatment. Arch Intern Med 1998;158(15):1617-1624.</li>
<li>Zimmerman RA, Bilaniuk LT. Computed tomographic staging of traumatic epidural bleeding. Radiology 1982;144(4):809-812.</li>
<li>de Andrade AF, Figueiredo EG, Caldas JG, et al. Intracranial vascular lesions associated with small epidural hematomas. Neurosurgery 2008;62(2):416-420; discussion 420-421.</li>
<li>Gean AD, Fischbein NJ, Purcell DD, Aiken AH, Manley GT, Stiver SI. Benign anterior temporal epidural hematoma: indolent lesion with a characteristic CT imaging appearance after blunt head trauma. Radiology 2010;257(1):212-218.</li>
<li>Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of acute epidural hematomas. Neurosurgery 2006;58(3 Suppl):S7-15; discussion Si-iv.</li>
<li>Glastonbury CM, Gean AD. Current neuroimaging of head injury. Semin Neurosurg 2003;14:79-88.</li>
<li>Hosoda K, Tamaki N, Masumura M, Matsumoto S, Maeda F. Magnetic resonance images of chronic subdural hematomas. J Neurosurg 1987;67(5):677-683.</li>
<li>Jaeger M, Meixensberger J. Traumatic subarachnoid hemorrhage and its clinical relevance. Intensivmed Notfallmedizin 2004;41(3):148-152.</li>
<li>Heit JJ, Iv M, Wintermark M. Imaging of intracranial hemorrhage. J Stroke 2017 Jan;19(1):11-27.</li>
<li>Chieregato A, Fainardi E, Morselli-Labate AM, Antonelli V, et al. Factors associated with neurological outcome and lesion progression in traumatic subarachnoid hemorrhage patients. Neurosurgery 2005;56(4):671-680.</li>
<li>Biedert S, Wolfsh&ouml;rndl H. Extraventricular obstructive hydrocephalus. Fortschr Neurol Psychiatr. 1994;62(11):405-408.</li>
<li>Verma RK, Kottke R, Andereggen L, et al. Detecting subarachnoid hemorrhage: comparison of combined FLAIR/SWI versus CT. Eur J Radiol 2013;82(9):1539-1545.</li>
<li>Winn W. <em>Youmans and Winn Neurological Surgery, 4-Volume Set.</em> 7th ed. Philadelphia, PA: Elsevier; 2016. https://www.elsevier.com/books/youmans-and-winn-neurological-surgery-4-volume-set/winn/978-0-323-28782-1. Accessed April 14, 2019.</li>
</ol>9772Breast Masses in Pregnancy and Lactation2019-04-29T13:15:16-04:002019-04-29T13:15:16-04:00Ida Teberian, M.D., Chandni Bhimani, D.O., Maria Sciotto, M.D., Annina Wilkes, M.D., Pauline Germaine, D.O.<p>Palpable breast lumps during pregnancy and lactation are a common presenting symptom. It is important to recognize benign masses to avoid unnecessary biopsies while maintaining a high clinical suspicion, as 20% of palpable lumps during this period are malignant.<sup>1</sup></p>
<p>This article will cover the imaging appearances of various benign and malignant masses that may occur during pregnancy and/or lactation on ultrasound, mammography, and MRI.</p>
<h2>Physiologic Changes in the Breast During Pregnancy and Lactation</h2>
<p>The breast undergoes physiologic changes during pregnancy and lactation due to hormonal stimulation that increases breast size and water content. These changes manifest clinically as increased nodularity and firmness, making it difficult to pinpoint a new palpable finding on self-breast and clinical exam. The breasts return to their normal baseline state 3 months after lactation has ceased.<sup>2</sup></p>
<p>When clinical concern arises, imaging is crucial for further evaluation. Ultrasound has the highest sensitivity and should be performed first. Mammography is less sensitive during this time due to the increased parenchymal density, which may obscure suspicious findings. This is most problematic in the late third trimester and during lactation.<sup>3</sup> Radiologists must be aware of the normal sonographic appearance of the breast during pregnancy and lactation. During pregnancy, the breasts demonstrate homogeneous hypoechogenicity. The lactating breast, however, demonstrates diffuse hyperechogenicity, as well as prominent ducts and increased vascularity.<sup>1-3 </sup>Contrast-enhanced MRI should be avoided in pregnancy if possible but is acceptable during lactation, although sensitivity will be decreased. Normal lactational tissue demonstrates diffusely increased T2 signal due to the increased water content as well as rapid and plateau enhancement kinetics of breast parenchyma.<sup>2,3</sup></p>
<h2>Breast Masses Unique to Pregnancy and Lactation</h2>
<h3>Lactating Adenoma</h3>
<p>Lactating adenomas are benign masses that arise in response to hormonal changes during pregnancy and lactation. They are common, representing 70% of biopsied masses in this population.<sup>4</sup> Lactating adenomas are similar to fibroadenomas but exhibit unique histologic features, most importantly the lack of both stromal components and myoepithelial proliferation. They are comprised of clusters of secretory lobules whose acini contain abundant secreted material including proteins, lipids and colostrum.<sup>1,3</sup></p>
<p>Lactating adenomas most commonly arise as a single mass that is palpable and mobile, although they can be multiple and bilateral. They often present during lactation and rarely prior to the third trimester of pregnancy. Uniquely, they can regress spontaneously after return to a nonlactating state.<sup>1</sup></p>
<p>Lactating adenomas share the same imaging appearance as fibroadenomas, with the most common sonographic appearance being a homogeneously hypoechoic solid mass with circumscribed margins and parallel orientation (<strong>Figure 1</strong>). Like fibroadenomas, they can develop areas of infarction due to rapid growth. They can have hypoechoic or hyperechoic areas due to fat content or lactational hyperplasia, respectively, or anechoic regions representing fluid. Suspicious features are also possible, including posterior acoustic shadowing, predominant hypoechogenicity, irregular shape, and microlobulated or indistinct margins, some of which may be secondary to infarction. When seen on mammography, they appear as a circumscribed mass with variable density, including low (fat) density, and may also have a fat-fluid level due to colostrum within secretory lobules.<sup>1</sup></p>
<p>Management is with close imaging surveillance if it appears benign. If it is atypical and without internal fat, biopsy should be performed. Lactating adenomas do not recur after surgical excision.<sup>5</sup></p>
<h3>Galactocele</h3>
<p>Galactocele is the most common benign breast mass in a lactating patient, although it more commonly presents after cessation of breastfeeding. It may also present in the third trimester of pregnancy. Galactocele is a retention cyst originating from an obstructed duct.<sup>2</sup> The contents are widely variable, with different proportions of fat, proteins, and lactose possible. Histologically, they demonstrate normal epithelium and myoepithelium.<sup>3</sup> A fibrous wall of variable thickness may be present due to inflammation as inflammation is often the cause of duct obstruction.<sup>1</sup> Galactoceles can also be associated with necrotic debris if there is leakage, which incites an inflammatory reaction resulting in fat necrosis.</p>
<p>Clinically, galactocele often presents as a painless palpable mass discovered after cessation of breastfeeding. If it is discovered while the patient is still lactating, a history of decreased frequency of breast-feeding is often elicited.<sup>3</sup> Galactoceles can be multiple and bilateral.<sup>4</sup></p>
<p>The imaging appearance of galactoceles varies depending upon cyst contents. On mammography, it often demonstrates radiolucency, although this depends on the amount of fat present. It can be completely lucent, in which case it is known as a pseudolipoma.<sup>2,5</sup> Alternatively, it may have high density if it contains more viscous fluid. On ultrasound, it most commonly looks like a complicated cyst. An important radiologic sign classically seen on ultrasound is a cyst with a fat-fluid level, which occurs in galactoceles with fresh milk content (<strong>Figure 2A</strong>). This can also be visualized on mammography on the mediolateral (ML) projection. Galactoceles with older milk content have higher viscosity and the fat and water do not separate, resulting in a similar imaging appearance to a fibroadenolipoma.<sup>2 </sup>Galactoceles may also appear as a solid mass with circumscribed margins and posterior acoustic enhancement, similar to a fibroadenoma, although a galactocele may also contain echogenic contents representing fat. With superimposed infection, it will appear as a complex cystic and solid mass. It is important to note that vascularity should never be present within the mass (<strong>Figure 2B</strong>).</p>
<p>With classic imaging and clinical features, no further intervention is required as galactoceles may regress spontaneously. Aspiration can be both diagnostic and therapeutic and will yield milky fluid, which may be thickened if performed after lactation has ended. Aspiration of milk must be accompanied by an appropriate clinical and imaging presentation to make the diagnosis, as similar fluid can be aspirated in any mass with lactational changes.<sup>2</sup></p>
<h3>Mastitis and Abscess</h3>
<p>Mastitis with or without an abscess occurs more commonly during lactation and is uncommon during pregnancy. Retrograde dissemination of infectious organisms from the baby&rsquo;s nose or throat occurs through disruption of skin at the nipple areola complex. The most common causative organisms are <em>Staphylococcus</em> and<em> Streptococcus</em>.<sup>2</sup></p>
<p>The diagnosis is most often clinical although imaging is indicated if an abscess or malignancy is suspected. Sonographic findings of simple mastitis include inflammation and periductitis. An abscess appears as an irregular hypoechoic or anechoic mass or complex cystic solid mass, with possible fluid or debris and posterior acoustic enhancement (<strong>Figure 3</strong>). Mammography is performed if there is suspicion of cancer, although it is often unrevealing due to increased parenchymal density. There may be skin and trabecular thickening due to edema and possibly a mass if there is an abscess.</p>
<p>Management of breast abscess includes diagnostic and therapeutic aspiration and appropriate antibiotic therapy, as well as surgical debridement if indicated, such as with a persistent or recurrent abscess or if it is &gt; 3 cm.<sup>4</sup> If after appropriate therapy the findings do not resolve, cancer should be suspected and further workup performed.</p>
<h2>Breast Masses That May Occur During Pregnancy and Lactation</h2>
<h3>Other Common Breast Masses in Pregnancy</h3>
<p><em>Fibroadenoma</em></p>
<p>Fibroadenomas are the most common tumor seen during pregnancy and lactation as they often undergo sudden growth secondary to hormonal stimulation, making them newly palpable. Rapid growth also results in susceptibility to infarction as they outgrow their vascular supply. This manifests clinically as new focal pain<sup> </sup>with possible adherence to the skin and reactive adenopathy.<sup>1,2</sup></p>
<p>Fibroadenomas arise in the terminal ductal-lobular unit (TDLU) and contain epithelial and stromal components. Secretory or lactational changes can be observed during pregnancy and lactation, whereas hyalinization, calcification, and ossification are atypical, classically occurring in older lesions in postmenopausal women.</p>
<p>The imaging appearance is usually identical to fibroadenomas in nonpregnant, nonlactating patients (<strong>Figure 4</strong>). A more complex appearance is possible during pregnancy, with cystic areas and/or prominent ducts, as well as greater vascularity. This may be due to infarction, which can also result in more lobulated margins, more heterogeneous echogenicity, and posterior acoustic shadowing.<sup>1</sup></p>
<p>Nonpalpable fibroadenomas and those previously present with up to 20% growth in size can undergo close surveillance. Any atypical appearance or new mass should undergo histologic analysis. Diagnosis can be made with fine-needle aspiration (FNA) or core needle biopsy, as discussed below in &ldquo;Tissue sampling during pregnancy and lactation.&rdquo; It is important to keep in mind that in fibroadenomas with secretory or lactational hyperplasia, milk can be aspirated, and calcifications may be present.<sup>2</sup></p>
<p><em>Cysts</em></p>
<p>Cysts and fibrocystic changes are benign entities that occur with the same frequency during pregnancy and lactation as they do outside of these conditions. They are an important consideration in the differential diagnosis of palpable masses in pregnant and lactating women as they are most common in young premenopausal women.<sup>4</sup></p>
<p>Cysts form either due to duct obstruction or an imbalance between secretions and absorption. Fibrocystic change represents various benign changes of ducts and stroma, such as adenosis, apocrine metaplasia, and usual ductal hyperplasia. It can present as cyclical breast pain and/or a palpable lump.</p>
<p>Cysts appear as circumscribed, homogeneous masses on mammography. Ultrasound is diagnostic, demonstrating an anechoic, round or oval mass with an imperceptible wall and posterior acoustic enhancement (<strong>Figure 5</strong>). In the case of complicated cysts, it is important to adhere to stringent diagnostic criteria, including round or oval shape, uniform hypoechogenicity or fine internal echoes, circumscribed margins, posterior acoustic enhancement, and lack of a perceptible wall. Management of complicated cysts in pregnancy and lactation includes close surveillance or aspiration, as the differential diagnosis includes galactocele and abscess.<sup>1 </sup>The MRI appearance of cysts is a uniformly T2-hyperintense, round or oval, nonenhancing mass.</p>
<p>Clustered microcysts represent a benign sonographic finding most often reflecting either fibrocystic change or apocrine metaplasia and are most common in perimenopausal women.<sup>4</sup> The typical appearance is a mass consisting of a group of 1-7 mm cysts with thin septae and lack of a solid component. They may be round, oval, or microlobulated and have circumscribed margins. They can contain debris as well as milk of calcium. MRI will show T2 hyperintensity with nonenhancing hypointense septations.<sup>4</sup> If there are any atypical features, including a solid component, indistinct margins, rapid growth, or suspicious calcifications, biopsy should be performed.</p>
<p>Fibrocystic change has various sonographic appearances, including complicated cyst and clustered microcysts. Less commonly, it can appear as a thick-walled cystic mass with posterior acoustic shadowing due to fibrosis. On mammography, it is often occult but may be seen as a focal asymmetry or circumscribed mass similar to a cyst. MRI can show cysts, rim-enhancing cysts, scattered enhancing foci, or focal or regional nonmass enhancement.<sup>4</sup></p>
<p>FNA can be performed for a symptomatic cyst for therapeutic relief. If cyst diagnosis is not certain based on imaging features, FNA can be performed to resolution to confirm that the finding is a cyst. If the cyst does not fully aspirate or a solid component persists, core biopsy should be considered.</p>
<h3>Other Breast Masses Not Unique to Pregnancy</h3>
<p><em>Intraductal Papilloma</em></p>
<p>Intraductal papilloma is a benign tumor representing papillary proliferation of ductal epithelium surrounding a fibrovascular stalk. Papillomas occur most often in women ages 30 to 50 years but are rare, accounting for 0.7% to 4% of solid breast lesions.<sup>4</sup> It can be solitary or multiple, with the solitary type usually in the central and retroareolar breast and in older patients, compared to multiple papillomas, which are usually peripheral and in younger patients.<sup>4,6</sup> They confer a slightly elevated risk of breast cancer, with a greater risk associated with multiple papillomas. The elevated risk is equal in both breasts.<sup>7</sup> Additionally, papillomas may be associated with atypia and ductal carcinoma in situ (DCIS), which are also more common with multiple papillomas.</p>
<p>Solitary papillomas present with bloody or nonbloody nipple discharge in 75% of cases. Bloody discharge occurs in cases of infarction and necrosis.<sup>4,5</sup> Multiple papillomas can present as palpable masses or with nipple discharge.</p>
<p>Ultrasound is more sensitive than mammography in detecting papillomas, which classically appear as a complex cystic and solid mass, representing growth within a duct (<strong>Figure 6</strong>). They may also appear as solid masses, similar to fibroadenomas. A feeding vessel may be identified, but it is important to keep in mind that lack of flow does not exclude the diagnosis.<sup>4</sup> This is especially important in pregnant and lactating women, as inspissated material within a focally dilated duct can mimic a papillary mass. Mammography may demonstrate a cylindrical, round, or oval mass, a focal asymmetry, or calcifications, which are present in 25%.<sup>7 </sup>MRI may depict a dilated duct containing an oval, enhancing mass, although irregular or spiculated margins and heterogeneous enhancement are also possible. The kinetic enhancement patterns are variable.<sup>4</sup> MRI has high sensitivity for detecting papillomas since they are typically vascular.</p>
<p>Diagnosis is made by core biopsy. The differential diagnosis includes papillary carcinoma, which is rare and most often occurs in postmenopausal women, and invasive ductal carcinoma with central necrosis and/or duct extension. Benign papillomas can undergo surveillance or be surgically excised. When associated with symptoms or atypia on pathology, they are likely to be excised.</p>
<p><em>Pseudoangiomatous Stromal Hyperplasia (PASH)</em></p>
<p>Pseudoangiomatous stromal hyperplasia (PASH) is an idiopathic benign proliferation of nonspecialized stroma separating breast lobules and ducts, which contains spindle cells that form clefts or spaces mimicking vascular spaces. This mesenchymal proliferation can be found as a microscopic focus or can form a mass, which can be palpable. PASH occurs in premenopausal women as it is hormone-sensitive. It is more often found microscopically in older patients and is rarely palpable in this population.<sup>5,8</sup> Although benign, PASH is associated with other benign or malignant masses in 23% of cases.<sup>8</sup></p>
<p>PASH has no specific imaging features and often resembles other masses, both benign and malignant (<strong>Figure 7</strong>). When it forms a mass, it is usually circumscribed with a round or oval shape and variable size. Mammography may depict a focal asymmetry or mass with no associated calcifications. If calcifications are present, they are due to a separate associated diagnosis. The mass is hypoechoic on ultrasound, usually with smooth margins and variable posterior sound transmission. MRI is equally nonspecific, demonstrating a mass or nonmass enhancement with variable T1 and T2 signal properties, although benign type 1 kinetics are most common. A suggestive MRI appearance is a mass containing T2-hyperintense slit-like spaces and cystic components.<sup>8</sup></p>
<p>Due to its nonspecific imaging appearance, PASH is a pathologic diagnosis. Clinically and radiologically it mimics fibroadenomas. Histologically, it can mimic low-grade angiosarcoma, which occurs predominantly in young women. Diagnosis of low-grade angiosarcoma can be made by identifying red blood cells within true vascular spaces and testing for endothelial cytologic markers.<sup>8</sup></p>
<p>Treatment of PASH is controversial although many agree that surgical excision is not necessary if pathology is concordant, in which case close surveillance is recommended.<sup>4,8</sup> Masses can grow over time and lead to discomfort or pain, in which case they are excised. Excision is also recommended in patients with a strong family history of breast cancer. Complete surgical excision is often performed in asymptomatic, average-risk patients due to the possibility of local recurrence and associated atypia, carcinoma in situ, or invasive carcinoma.<sup>8-10</sup></p>
<p><em>Granulomatous Mastitis</em></p>
<p>Granulomatous mastitis is a very rare idiopathic inflammatory disease that has an association with pregnancy, with most patients presenting at a young age and usually within 5 years of pregnancy.<sup>2</sup> Clinical presentation may be with solitary or multiple firm palpable masses and possible associated lymphadenopathy or a more diffuse process.<sup>11</sup> There is no predilection for a specific location, although the subareolar breast is often spared.<sup>2,4</sup></p>
<p>Mammograms are often normal but the most common finding is a focal asymmetry (<strong>Figure 8A</strong>).<sup>2</sup> It can also present as a mass with variable features. Ultrasound may show the classic appearance of multiple clustered tubular hypoechoic lesions, possibly with an associated hypoechoic mass (<strong>Figures 8B-F</strong>).</p>
<p>The diagnosis is one of exclusion as the histologic features are nonspecific, consisting of a noncaseating, nonvasculitic granulomatous reaction centered around breast lobules. The differential diagnosis for this is large and includes fungal and tuberculous infections, sarcoidosis, and a granulomatous reaction to carcinoma.<sup>2,4</sup></p>
<p>Prognosis is good despite the possibility of local recurrence with surgical excision and corticosteroid therapy. If an organism is isolated, antibiotic therapy can be effective.<sup>2,4,11</sup></p>
<p><em>Juvenile Papillomatosis</em></p>
<p>Juvenile papillomatosis is a very rare benign proliferative disorder that occurs more frequently during pregnancy and lactation as it is affected by hormonal stimulation. It consists of multiple cysts and dilated ducts within a dense fibrous stroma and clinically presents as a firm, mobile mass often at the periphery of the breast, mimicking fibroadenomas.<sup>12</sup> It is associated with increased risk of breast cancer, which may be concurrent with the diagnosis in 5% to 15% of cases and is considered a marker for familial breast cancer as 33% to 58% of patients have a positive family history.<sup>9,12</sup></p>
<p>Ultrasound classically demonstrates an ill-defined hypoechoic mass comprised of multiple small anechoic cysts, often peripherally located (<strong>Figure 9</strong>). Mammograms are nonspecific and often negative but may show microcalcifications or an asymmetry. The MRI appearance is a lobulated mass containing small internal cysts with marked contrast enhancement with benign-type kinetics.<sup>9,12</sup></p>
<p>Treatment is by surgical excision with wide margins as local recurrence is a possibility and because of the possible association with malignancy. Annual clinical surveillance after excision is recommended, as well as surveillance of family members.</p>
<p><em>Fibroadenolipoma (Hamartoma)</em></p>
<p>Fibroadenolipomas are benign masses containing glandular, stromal, and adipose tissue, the three components of a normal breast. They may occur at any point in a woman&rsquo;s life, including pregnancy and lactation, although there is no predilection for a certain physiologic state. They may present as palpable, soft, painless lumps.</p>
<p>Imaging by mammography and ultrasound depicts characteristic findings. On mammography and ultrasound both fat and parenchymal densities are seen within a circumscribed mass, often termed a &ldquo;breast within a breast&rdquo; appearance (<strong>Figure 10</strong>). Similar to other benign masses during pregnancy and lactation, growth and/or infarction can occur, resulting in atypical features.<sup>1</sup> With atypical sonographic features, mammographic demonstration of fat density can be helpful. Ultimately, biopsy must be performed if there is any uncertainty.</p>
<p><em>Breast Cancer </em></p>
<p>Pregnancy-associated breast cancer (PABC) is defined as breast cancer diagnosed during pregnancy or within 1 year of childbirth. It is rare, occurring in 1 out of 3,000 to 10,000 pregnancies and constituting 3% of all breast cancers.<sup>2,4</sup> It accounts for 6% to 10% of all cancers in women under 40, with the average age of onset at 34 years old.<sup>1 </sup></p>
<p>Patients usually present in the postpartum period, with 20% occurring during pregnancy.<sup>1</sup> Clinical presentation is usually with a large palpable mass and lymphadenopathy (<strong>Figure 11</strong>). Patients may also present with locally advanced disease, manifesting as swelling, erythema, and enlargement of the breast. The disease is more advanced at presentation compared to nonpregnancy-associated breast cancer in women of the same age. Tumors are more commonly high-grade, more than half present with metastatic lymphadenopathy, and inflammatory cancer is more common. Interestingly, approximately one-third of malignancies occur in high-risk women.<sup>1</sup></p>
<p>Imaging features are similar to nonpregnancy-associated malignancy and can be benign-appearing, typical of high-grade tumors, demonstrating posterior acoustic enhancement on ultrasound.<sup>1</sup> Mammography is performed as it depicts calcifications, present in up to 55% of cases,<sup>2</sup> and may show multifocal or multicentric disease.</p>
<p>Treatment during pregnancy and lactation has some important considerations. Chemotherapy can be administered during the second and third trimesters with the primary fetal risk being prematurity. Radiation and hormone therapy are contraindicated during pregnancy.<sup>1 </sup>Surgery can usually be performed at any point during pregnancy, although waiting until after the first trimester may be appropriate in certain cases.</p>
<p><em>Lymphoma</em></p>
<p>Primary breast lymphoma (PBL) is very rare, representing 0.1% of breast cancers, and occuring mostly in women in their fifth and sixth decades.<sup>4,13</sup> It is a form of non-Hodgkin lymphoma (NHL) and most often of B cell lineage. Burkitt lymphoma of the breast (BLB) is a very rare B-cell NHL subtype, which can be endemic, occurring in young African patients, or sporadic, occurring in Europe and the US. The sporadic form is most common and has been associated with pregnancy and the postpartum period, sometimes referred to as pregnancy-related Burkitt lymphoma.<sup>2</sup></p>
<p>Patients with PBL often present with either a discrete palpable, painful mass or diffuse thickening.<sup>4,14</sup> There is no skin or nipple retraction or nipple discharge and patients rarely experience typical B symptoms (fever, weight loss, and night sweats). There can be diffuse breast enlargement with edema, mimicking inflammatory breast cancer. BLB often causes massive enlargement of both breasts.<sup>2</sup> It is aggressive and infiltrative, causing increased parenchymal density. Findings elsewhere in the body include enlargement of both ovaries and other abdominal organs. Peripheral lymph nodes are rarely involved.<sup>2</sup></p>
<p>Imaging is nonspecific. A solitary mass is more common than multiple masses, which only occur in 9% of cases and is more common in secondary breast lymphoma (SBL).<sup>13</sup> Mammography may be negative or may show masses or global asymmetry. Mass margins can be indistinct or circumscribed. There are no associated calcifications or architectural distortion. Global asymmetry is seen in one-third of patients and is often associated with high-grade lymphoma.<sup>2,13</sup> There are often associated enlarged axillary lymph nodes. Ultrasound is nonspecific and variable, often demonstrating a round or oval hypoechoic mass with circumscribed or indistinct margins and variable vascularity and posterior acoustic properties, although up to 64% have hypervascularity and up to 75% have posterior enhancement (<strong>Figure 12</strong>).<sup>13</sup> There are often overlying skin changes as it is spread through the lymphatics.<sup>14</sup> Lymphoma on MRI is irregular with mild-to-marked heterogeneous enhancement and restricted diffusion.</p>
<p>PBL is aggressive with high relapse rates, occurring in the CNS in 20% of patients.<sup>13</sup> Treatment is primarily with chemoimmunotherapy and radiation, with surgical treatment offering no benefit.<sup>13,15</sup> Pregnancy-related BLB often spreads rapidly, has a poor prognosis, and can be easily misdiagnosed without adequate immunophenotypic or chromosome analysis.<sup>2,16</sup> Interestingly, it has also been known to spontaneously regress after cessation of lactation.<sup>2</sup></p>
<p><em>Metastatic Disease</em></p>
<p>Metastases to the breast are rare although they are the first manifestation of the primary malignancy in up to 50% of cases.<sup>14</sup> The most common secondary breast malignancies are lymphoma, melanoma, lung and ovarian cancer, and sarcomas.<sup>4</sup> They can present as rapidly growing, painless masses but most are asymptomatic.<sup>17</sup> Prognosis is poor with median survival of 10 months.<sup>18</sup></p>
<p>Metastases that have spread hematogenously present as masses, whereas those with lymphatic spread result in more diffuse findings similar to lymphoma. Solitary masses are more common, but metastases are more likely to be multiple and bilateral than primary breast cancer (<strong>Figure 13</strong>). They classically lack signs of a desmoplastic reaction (spiculation, skin/nipple retraction). They are most often in areas of rich blood supply, including the upper outer quadrant, superficial subcutaneous tissue, and edges of breast parenchyma.<sup>14,18</sup> Masses are usually round and circumscribed and rarely cause distortion or contain calcifications. Calcifications can be found with certain malignancies, such as ovarian cancer. Mammographically, the masses are usually high-density with indistinct or microlobulated margins. Most masses are hypoechoic or heterogeneous but can be hyperechoic. They often have posterior enhancement and posterior shadowing is uncommon. Vascularity is variable and depends on the primary tumor.<sup>18</sup> Lymphatically spread malignancy will appear as diffuse heterogeneously hyperechoic adipose and glandular tissue with skin thickening and adenopathy. Although it mimics inflammatory breast cancer, there is no associated mass. MRI will often show T1 and T2 isointensity except for melanoma, which will be T1-hyperintense. Metastases often demonstrate rapid homogeneous enhancement with plateau or washout kinetics.<sup>4,14,17,18</sup></p>
<h2>Tissue Sampling During Pregnancy and Lactation</h2>
<p>FNA and core needle biopsy are options for tissue sampling. Core needle biopsy has a high sensitivity and specificity, allowing for a more definitive and confident diagnosis.&nbsp;Core needle biopsy also allows for ancillary testing such as for immunochemistry for estrogen and progesterone receptors in a malignancy, which would not be possible in the setting of FNA; this would be especially important in a BIRADS 4C or BIRADS 5 finding.<sup>22,23</sup></p>
<p>Due to increased vascularity in pregnancy, there is a slightly higher risk of bleeding and infection. Subcutaneous lidocaine has no known harmful effects to the fetus and is safe to use during pregnancy and lactation.<sup>7</sup></p>
<p>Milk fistula is rarely a complication of core needle biopsy. Using an oblique track from skin surface to the target for biopsy can help decrease the incidence of milk fistula. If it occurs, it usually resolves on its own in several weeks. If it does not resolve, it may be necessary to suppress lactation to close the fistula.<sup>22,23</sup></p>
<h2>Conclusion</h2>
<p>Palpable lumps can be a diagnostic challenge during pregnancy and lactation, both clinically and radiologically. Radiologists must be aware of the appearance of normal physiologic changes as well as the various entities that may present in this population. Biopsy during pregnancy and lactation carries greater risk of bleeding, infection, and fistula formation and can be avoided with adequate knowledge of the diagnostic imaging signs of common benign diagnoses. It is equally imperative to be aware of atypical findings and proceed to biopsy when they are present, however, as pregnancy-associated malignancy carries a poor prognosis that worsens with delayed diagnosis.</p>
<h2>References</h2>
<ol>
<li>Langer A, Mohallem M, Berment H, et al. Breast lumps in pregnant women. Diagn Interv Imaging 2015;96:1077-1087.</li>
<li>Sabate JM, Clotet M, Torrubia S, et al. Radiologic evaluation of breast disorders related to pregnancy and lactation. Radiographics 2007;7:S101-S124.</li>
<li>Vashi R, Hooley R, Butler R, et al. Breast imaging of the pregnant and lactating patient: physiologic changes and common benign entities. Am J Roentgenol 2013;200(2):329-336.</li>
<li>Kopans DB. Breast Imaging, 3rd ed. Baltimore, MD: Lippincott Williams &amp; Wilkins, 2007.</li>
<li>Rosen P. Rosen&rsquo;s Breast Pathology. 2d ed. New York: Lippincott Williams and Wilkins; 2001.</li>
<li>Yu JH, Kim MJ, Cho H, et al. Breast diseases during pregnancy and lactation. Obstet Gynecol Sci 2013;56(3):143-159.</li>
<li>Vashi R, Hooley R, Butler R, et al. Breast imaging of the pregnant and lactating patient: imaging modalities and pregnancy-associated breast cancer. Am J Roentgenol 2013;200(2):321-328.</li>
<li>Hosny IA, Salah El Din LA, Elghawabi HS. Radiological evaluation of palpable breast masses during pregnancy and lactation. Egyp J Radiol Nucl Med 2011;42:267-273.</li>
<li>Eiada R, Chong J, Kulkarni S, et al. Papillary lesions of the breast: MRI, ultrasound, and mammographic appearances. Am J Roentgenol 2012;198:264-271.</li>
<li>Brookes MJ, Bourke AG. Radiological appearances of papillary breast lesions. Clin Radiol 2008;63:1265-1273.</li>
<li>Raj SD, Sahani VG, Adrada BE, et al. Pseudoangiomatous stromal hyperplasia of the breast: multimodality review with pathologic correlation. Curr Probl Diagn Radiol 2017;46:130-135.</li>
<li>Chung EM, Cube R, Hall GJ, et al. From the archives of the AFIP: breast masses in children and adolescents: radiologic-pathologic correlation. Radiographics 2009;29:907-931.</li>
<li>Valeur NS, Rahbar H, Chapman T. Ultrasound of pediatric breast masses: what to do with lumps and bumps. Pediatr Radiol 2015;45:1584-1599.</li>
<li>Ogawa T, Mizutani M, Yabana T, et al. Case report: a case of Burkitt&rsquo;s lymphoma involving both breasts. Breast Cancer 2005;12(3):234-237.</li>
<li>Liu M, Hsieh C, Wang A, et al. Primary breast lymphoma: a pooled analysis of prognostic factors and survival in 93 cases. Ann Saudi Med 2005; 25(4):288-293.</li>
<li>Surov A, Fiedler E, Holzhausen H, et al. Metastases to the breast from non-mammary malignancies: primary tumors, prevalence, clinical signs, and radiological features. Acad Radiol 2011;18:565-574.</li>
<li>Sippo DA, Kulkarni K, DiCarlo P, et al. Metastatic disease to the breast from extramammary malignancies: a multimodality pictorial review. Curr Probl Diagn Radiol 2016;45:225-232.</li>
<li>Bitencourt AGV, Gama RRM, Graziano L, et al. Breast metastases from extramammary malignancies: multimodality imaging aspects. Br J Radiol 2017; 90:20170197.</li>
<li>Parker S, Saettele M, Morgan M, et al. Spectrum of pregnancy- and lactation-related benign breast findings. Curr Probl Diagn Radiol 2017;46:432-440.</li>
<li>Lepori D. Inflammatory breast disease: the radiologist&rsquo;s role. Diagnostic and Interventional Imaging 2015;96:1045-1064.</li>
<li>Glazebrook KN, Magut MJ, Reynolds C. Angiosarcoma of the breast. Am J Roentgenol 2008;190:533-538.</li>
<li>Mitra S and Dey P. Fine-needle aspiration and core biopsy in the diagnosis of breast lesions: a comparison and review of the literature. Cytojournal 2016;13:18.</li>
<li>Mahoney MC and Ingram AD. Breast emergencies: types, imaging features, and management. Am J Roentgenol 2014;202:W390-W399.</li>
</ol>9770Fibroadenoma: From Imaging Evaluation to Treatment2019-04-29T13:00:53-04:002019-04-29T13:00:53-04:00Kimberly Klinger, M.D., M.S.H.A., Chandni Bhimani, D.O., Jason Shames, M.D., M.B.S., Alexander Sevrukov, M.D.<h2>Background and Epidemiology</h2>
<p>Fibroadenoma is the most common benign breast tumor in women younger than age 30. They present most frequently between ages 20 and 50 with peak incidence reported at 20 to 24 years.<sup>1</sup> They account for 68% of all breast masses and a large proportion of breast biopsies.<sup>2</sup></p>
<p>Fibroadenomas most commonly present as a single, painless, firm, mobile mass, but can be multiple in up to 25% of patients (<strong>Figure 1</strong>).<sup>2</sup> There is a wide spectrum of associated symptoms, from asymptomatic to extremely painful and cosmetically distorting.</p>
<p>Risk factors for fibroadenoma include age &lt; 35 years, history of benign breast disease, and breast self-examination.<sup>2</sup> The incidence of fibroadenoma has also been shown to directly correlate with body mass index (BMI), with peak incidence seen with BMI 25 to 29.9 kg/m.<sup>2</sup> Increased parity and the use of oral contraceptives appear to decrease fibroadenoma risk.<sup>2</sup></p>
<h2>Pathophysiology and Natural History</h2>
<p>Fibroadenomas arise from the lobular stroma of the terminal duct lobular unit. They are a proliferation of epithelial and stromal components, likely related to estrogen. Over time, if left in situ, they undergo hyalinization of the stromal component with regression of the epithelial component.<sup>1</sup></p>
<p>They are hormone-responsive masses and may undergo cyclic changes in size and symptoms with menses. As such, they increase in size during pregnancy and lactation and are the most common breast tumor diagnosed during pregnancy and the peripartum period.<sup>3</sup> Upon hormone withdrawal during menopause, fibroadenomas commonly involute.</p>
<p>The natural history of fibroadenomas varies from patient to patient with some remaining stable, others demonstrating growth, and others regressing. Most commonly, fibroadenomas decrease in size over time as they lose cellularity. Calcifications can form within the hyalinized or necrotic stroma of involuting fibroadenomas, classically described as coarse, &ldquo;popcorn-like&rdquo; calcifications.<sup>4</sup> Malignant transformation of fibroadenomas is rare, occurring in less than 0.3%.<sup>2</sup></p>
<h2>Classic Imaging Features of Fibroadenoma</h2>
<h3>Mammogram</h3>
<p>Fibroadenomas are oval, or less frequently round, equal density masses on mammogram with a circumscribed or obscured margin. Oval fibroadenomasoften have lobulations. A dark halo around the mass can be seen due to an optical illusion known as the Mach effect caused by an inbuilt edge enhancement mechanism of the human retina.<sup>5</sup> Calcifications can form within an involuting fibroadenoma and are detectable on mammogram, typically in postmenopausal women.<sup>4</sup> Calcification typically starts at the periphery of the mass and coalesces centrally. Fibroadenoma calcifications can range in morphology from round to coarse dystrophic to pleomorphic (<strong>Figure 2B-C</strong>). When beginning to calcify, fibroadenomas may appear suspicious, necessitating further imaging evaluation and biopsy. In a postmenopausal patient, when the calcifications are coarse and &ldquo;popcorn-like,&rdquo; the diagnosis of involuting fibroadenoma can be made mammographically without further workup. However, a circumscribed mass with calcifications should not be dismissed as an involuting fibroadenoma in a premenopausal woman, as the differential includes cancer.<sup>6</sup> If the morphology of calcifications is suspicious, biopsy may be warranted (<strong>Figure 2D</strong>). Most often, mammographic features of fibroadenoma are nonspecific requiring further evaluation with ultrasound and possibly biopsy depending on sonographic findings.</p>
<h3>Contrast-enhanced Digital Mammography (CEDM)</h3>
<p>Fibroadenomas may or may not enhance on CEDM. When they do enhance, the level of enhancement is variable. The presence of enhancement may support biopsy, as malignancy typically enhances avidly on CEDM (<strong>Figure 3</strong>). However, the ultimate decision to biopsy must be based on ultrasound morphology.</p>
<h3>Ultrasound</h3>
<p>On ultrasound, fibroadenomas typically appear as oval, parallel, circumscribed, uniformly hypoechoic masses with echogenic, thin fibrous internal septations (<strong>Figure 1B, 2A</strong>) and variable posterior features. Posterior features depend on mass composition, with more hyalinized masses demonstrating posterior acoustic shadowing and epithelial dominant lesions exhibiting posterior enhancement. Associated calcifications can be seen in approximately 10% and are better characterized on mammography.<sup>1</sup> An echogenic rim, or pseudocapsule, surrounding the mass can be seen secondary to compression of adjacent breast stroma. Internal vascularity is seen in up to 80% on Doppler imaging (<strong>Figure 1B</strong>).<sup>1</sup> When imaging features are not classic (eg, irregular shape or indistinct or microlobulated margins) biopsy should be considered (<strong>Figure 4</strong>).</p>
<h3>MRI</h3>
<p>Similar to posterior characteristics on ultrasound, the appearance of a fibroadenoma on MRI varies based on the hyalinization of the mass. Hyalinized or sclerotic fibroadenomas appear T2 hypointense. In contrast, cellular or myxoid fibroadenomas are hyperintense on T2 and hypointense on T1-weighted sequences (<strong>Figure 5A-B</strong>). Fibroadenomas show variable enhancement patterns. Myxoid fibroadenomas demonstrate rapid homogeneous contrast enhancement whereas sclerotic fibroadenomas show little to no enhancement. Typical fibroadenomas follow type 1 enhancement kinetics: rapid initial and persistent delayed phases (<strong>Figure 5C</strong>). However, fibroadenomas may have a dynamic contrast enhancement pattern suggestive of malignancy in up to one-third of cases.<sup>7</sup> Classic fibroadenomas will have dark fibrous internal septations (<strong>Figure 5D</strong>). These nonenhancing septations are seen in 40% to 60% of fibroadenomas.<sup>1</sup> While suggestive of fibroadenoma, these septations are nonspecific and other imaging characteristics and clinical factors must be considered.</p>
<h2>Differential Considerations and Atypical Imaging Presentations</h2>
<p>Variants of fibroadenoma are important to consider, as their management differs slightly from typical fibroadenomas. A juvenile fibroadenoma is a variant seen primarily in adolescence. Apart from patient age, larger size, and characteristic rapid growth (<strong>Figure 6</strong>), these masses cannot be distinguished from typical fibroadenomas by imaging. At pathology, they are differentiated by the increased stromal hypercellularity of juvenile fibroadenomas.<sup>1</sup> In contrast to typical fibroadenomas, they are usually treated with excision given the rapid growth and larger size.</p>
<p>Another variant is a complex fibroadenoma. While these cannot be completely distinguished from fibroadenoma on imaging, sonographic features suggestive of a complex fibroadenoma include internal heterogeneity, cysts, and punctate echogenic foci. Awareness of these features is important because their presence may motivate biopsy in lieu of routine follow-up. Upon biopsy, complex fibroadenomas may demonstrate cysts, sclerosing adenosis, epithelial calcifications, or papillary apocrine changes.<sup>1</sup> Diagnosis of a complex fibroadenoma has been associated with an increased risk of invasive breast cancer for both breasts. Dupont et al showed that the relative risk of invasive breast cancer is 3.10 times higher for women with complex fibroadenomas compared to 2.17 times higher for patients with typical fibroadenomas.<sup>8</sup> However, a recent study performed by Nassar et al found that complex fibroadenomas do not confer increased risk of breast cancer beyond that of the established histologic features and should be managed based on the associated histologic findings.<sup>9</sup></p>
<p>Another key differentiation is that between fibroadenoma and phyllodes tumor, another fibroepithelial lesion of the breast. In contrast to fibroadenomas, phyllodes tumors, although rare, may have locally aggressive or frankly malignant potential and should be managed surgically.<sup>10</sup> Thus, the differentiation between the two is clinically significant. Fibroadenoma and phyllodes tumor share many common imaging findings and it is difficult to distinguish them on all breast imaging modalities (<strong>Figure 7A</strong>). The presence of intralesional clefts and cystic spaces on ultrasound may favor phyllodes tumor (<strong>Figure 7B</strong>).<sup>11</sup> However, these features have not been found reliably useful for differentiation. A study on MRI differentiation of these lesions found a nonsignificant difference in heterogeneous inner structure and nonenhancing septation, with phyllodes tumors displaying these features more often than biopsy-proven fibroadenomas.<sup>7</sup> In spite of these subtle differences, ultimately the study found that phyllodes tumors and fibroadenomas cannot be precisely differentiated on breast MRI. Diagnosis is further complicated by similar clinical presentation; however, phyllodes tumors tend to be diagnosed later in life compared with fibroadenomas, with a median age at presentation of 42 to 45 years.<sup>12,13</sup></p>
<p>In addition to phyllodes tumors, imaging features of fibroadenoma also overlap with other fibroepithelial lesions including tubular adenoma and lactational adenoma. Tubular adenomas are rare and found primarily in younger women. Tubular adenomas can have varied appearance related to the patient&rsquo;s age. In younger patients, they appear as a noncalcified, circumscribed, solid mass, similar to a fibroadenoma (<strong>Figure 8</strong>). In older patients, they can appear as suspicious, irregular masses with microcalcifications requiring core biopsy, although this is less common.<sup>14</sup></p>
<p>Lactational adenomas are a common solid breast mass diagnosed during pregnancy thought to arise due to the physiologic changes of pregnancy and lactation. Some regard this mass as a variant of fibroadenoma, tubular adenoma, or lobular hyperplasia that has undergone histologic changes as a result of the physiologic state induced by pregnancy (<strong>Figure 9</strong>).<sup>3</sup> They appear on ultrasound as oval, circumscribed, homogeneous, hypoechoic to isoechoic masses, indistinguishable from fibroadenomas. They may have hyperechoic areas, representing inspissated milk, and posterior enhancement secondary to the fluid component, which can serve as useful diagnostic signs on ultrasound.<sup>1,3</sup> On mammogram, they can have radiolucent areas representing the fat content of the milk secondary to lactational hyperplasia. Rarely, lactational adenomas can appear suspicious on ultrasound with irregular contours and posterior acoustic shadowing.<sup>3</sup> Lactational adenomas require tissue sampling or close surveillance with tissue sampling favored when imaging is atypical; although, there is a small risk for milk fistula after core biopsy.</p>
<p>While it is difficult to distinguish between the different benign fibroepithelial lesions on imaging, it can also be challenging to distinguish between fibroadenomas and malignant masses. Ultrasound features of BRCA-associated breast cancers can resemble a benign mass, such as a fibroadenoma. BRCA-associated breast cancer can appear as a round, circumscribed, hypoechoic and homogenous mass with increased through transmission (<strong>Figure 10A-B</strong>).<sup>15</sup> Knowing the patient&rsquo;s personal and family history and BRCA status, if tested, is crucial in determining management of a mass on mammogram, ultrasound, or MRI. What may look like a classic fibroadenoma in an average-risk patient may be a breast cancer in a BRCA-positive or other high-risk patient (<strong>Figure 10C-F</strong>). Thus, biopsy rather than periodic imaging follow-up is more readily performed for benign or probably benign masses in high-risk patients due to their increased lifetime risk of developing breast cancer.</p>
<p>MRI, one of the key screening modalities in the BRCA-positive population owing to its sensitivity, cannot reliably distinguish benign entities from malignancy. For example, fibroadenomas may have a dynamic contrast-enhancement pattern suggestive of malignancy in up to one-third of cases.<sup>7</sup> Additionally, mucinous carcinoma, which is typically T2 hyperintense, often mimics a probably benign lesion.<sup>7</sup> High-grade cancers may have circumscribed margins, a typically benign feature, due to fast cellular growth rates allowing minimal time for the reactive parenchymal changes that contribute to the appearance of a morphologically malignant, spiculated mass.</p>
<p>Breast-specific gamma imaging (BSGI) and its predecessor scintimammography are other modalities used primarily as adjunctive screening tools in high-risk women. When used with mammography for breast cancer screening in women at increased risk and with dense breasts, BSGI significantly improves sensitivity and positive predictive value. BSGI also increases the number of breast cancers detected, as it has been shown to detect mammographically occult breast cancer.<sup>16</sup> BSGI uses the radiotracer Tc-99m sestamibi to identify physiological differences between malignant and normal breast tissue.<sup>16</sup> Focally increased radiotracer uptake is the hallmark of malignancy on BSGI (<strong>Figure 11</strong>). However, fibroadenomas can present a diagnostic quandary. While generally &ldquo;cold&rdquo; on BSGI (<strong>Figure 12</strong>), fibroadenomas and other benign breast disease can appear &ldquo;hot&rdquo;, with increased radiotracer uptake relative to background (<strong>Figure 13</strong>), similar to other functional modalities, such as MRI and CEDM. In fact, fibroadenomas, fibrocystic disease and inflammatory lesions are regarded as well-known causes of false-positive Tc-99m sestamibi uptake. In these cases, dual-phase imaging in BSGI may help discriminate between benign and malignant lesions based on the assumption that Tc-99m sestamibi uptake by cancerous cells might persist on delayed images compared with benign conditions.<sup>17</sup> A recent study showed that in 11 false positive cases, 9 patients showed tracer washout one hour after tracer injection, supporting this notion.<sup>17</sup></p>
<h2>Treatment Options for Fibroadenoma</h2>
<p>If classic features of fibroadenoma are present, the lesion can be followed by imaging every 6 months for 2 years (or at 6, 12 and 24 months) without core biopsy. There is a growing body of evidence showing that periodic imaging surveillance is a safe management option for probable fibroadenomas. A study about long-term follow-up performed by Gordon et al reported that fibroadenomas may be safely followed with volume growth rates of up to 16% per month for patients &lt; 50 years old and up to 13% per month in those <u>&gt;</u> 50.<sup>18</sup> This study determined that the acceptable mean change in size for all ages was equivalent to a 20% increase in all 3 dimensions in a 6-month period.<sup>18</sup> If &gt; 20% growth is observed during the follow-up period, biopsy should be performed.</p>
<p>Choosing to biopsy a probable fibroadenoma is practice and patient specific. The patient&rsquo;s personal history, family history, and age are taken into account in conjunction with imaging features of the mass when deciding to biopsy. If any imaging features other than the classic features are present, or if the clinical presentation raises a concern for malignancy or a phyllodes tumor (rapid growth, new presentation after menopause, etc.), a biopsy is recommended. Fibroadenomas with epithelial abnormalities found at core biopsy require surgical excision, even though occurrence of malignancy in or adjacent to a biopsy-proven fibroadenoma is rare.<sup>19</sup> Fibroadenomas without epithelial abnormality diagnosed by core biopsy need no specific follow-up and can be left alone if asymptomatic. For symptomatic patients wanting definitive treatment for a fibroadenoma, options include surgical excision or minimally invasive techniques, such as ablative procedures and vacuum-assisted core biopsy. Generally, women with fibroadenomas measuring &gt; 3 cm are sent for surgical consultation.</p>
<h3>Surgical Excision</h3>
<p>Surgical excision is the most utilized strategy for definitive treatment of a fibroadenoma. Approximately 500,000 fibroadenomas are treated by surgical excision each year.<sup>20</sup> Surgery is the best option for a symptomatic woman and a consult should be considered. Giant fibroadenomas, also known as juvenile fibroadenomas, require surgical excision due to associated complications including breast distortion, potential for psychological harm, and rapid enlargement that may cause venous congestion, glandular distortion, pressure necrosis and ulceration.<sup>20 </sup>While surgery allows for complete resection, there are risks associated with general anesthesia as well as a greater potential for poor cosmetic outcomes requiring an additional reconstructive surgery. Given the nonmalignant nature of fibroadenomas, an important treatment goal should be cosmesis. A study by Cochrane et al found that the best cosmetic outcomes and highest patient satisfaction occurred when &lt; 10% of the breast volume was excised.<sup>21</sup> Minimally invasive surgical techniques, such as endoscopic lumpectomy, have been pursued for improved cosmesis. In this procedure, 3 small incisions are made in the midaxillary line, a trocar is inserted in the region of the tumor, and carbon dioxide gas is insufflated into the chest wall to facilitate tumor access. The tumor is then dissected and retrieved, either intact or piecemeal depending on initial size, with a specimen retrieval bag.<sup>20</sup> Endoscopic removal by this extramammary approach has been proposed as the best option for benign breast tumors, such as fibroadenomas, considering the young age of the patient population and the excellent cosmetic outcomes.<sup>22</sup> Nevertheless, open excision is still more common. Effort is also made to improve cosmesis in open breast-conserving surgery by making incisions in the circumareolar region or the inframammary crease.<sup>20</sup></p>
<h3>Minimally Invasive Techniques</h3>
<p>In addition to minimally invasive surgical approaches, minimally invasive office-based procedures have been used in treating fibroadenoma. Office-based techniques performed under local anesthesia lack the risks of general anesthesia and are relatively painless compared to open surgery. They also promise improved cosmetic outcomes, with little to no tissue loss during percutaneous ablative techniques. Office-based procedures are also more cost effective. Surgical techniques, however, have the advantage of allowing for additional pathologic analysis upon removal.</p>
<p><strong><i>Vacuum-Assisted Breast Biopsy&mdash;</i></strong>Small (&lt; 2 to 3 cm) fibroadenomas can be removed under image guidance using a vacuum-assisted device, similar to that used for vacuum-assisted core needle biopsy. Multiple samples are obtained with the needle until the mass appears completely removed. Complete excision is not guaranteed and hemorrhage and hematoma can result due to the multiple samples required for removal, especially when fibroadenomas are &gt; 2 cm. Hematoma formation occurs at a rate of 0% to 13%.<sup>20</sup> Removal of the lesion ranges from 22% to 98% depending on the quality of imaging technique, needle gauge, and initial size of the lesion.<sup>20</sup> This technique is not utilized for malignant lesions due to the risk of incomplete removal. Despite incomplete removal and resulting risk of recurrence, patients report high satisfaction with the procedure and prefer it to surgical excision.<sup>2</sup> The American Society of Breast Surgeons (ASBrS) endorses ultrasound-guided percutaneous excision of fibroadenomas in their 2008 statement as a safe, effective and well-tolerated procedure with minimal cost, low morbidity, and desirable cosmetic outcomes.</p>
<p><strong><i>Percutaneous Ultrasound-Guided Cryoablation&mdash;</i></strong>Percutaneous cryoablation is an FDA-approved non-surgical option for patients desiring definitive, minimally invasive treatment of a fibroadenoma. Cryoablation is also endorsed by the ASBrS in their 2008 statement as a safe and efficacious treatment for fibroadenoma. Careful patient selection is made using ASBrS criteria for cryoablation of fibroadenoma including the need for visibility by ultrasound, definitive histologic confirmation with core biopsy, and size &lt; 4 cm. Although it is a well-accepted treatment option in the medical community, cryoablation is not widely utilized as many insurance companies categorize it as investigational.</p>
<p>Cryoablation systems use a cooling gas under pressure inside a shielded probe to freeze adjacent tissue. Real gases change temperature relative to pressure when forced through a valve and heat exchange with the environment is prevented. This principle is known as the Joule-Thomson Effect, or throttling process, and is the basis of cryoablation systems. The amount and direction of temperature change depends on the Joule-Thomson coefficient of a gas, which represents the rate of temperature change relative to pressure. Nitrogen or argon gas is used most commonly in cryoablation systems based on their favorable coefficients.</p>
<p>During the procedure, a 9- or 10-gauge cryoablation probe is inserted into the center of the breast tumor under real-time sonographic guidance after administration of local anesthesia. High-pressure gas is forced through the center chamber of the dual-chambered probe. At the tip of the probe, the gas enters the expansion chamber where pressure decreases and the gas cools. The cold gas absorbs heat energy from the surrounding tissue via conduction, lowering tissue temperature and freezing the adjacent tissue, creating an &ldquo;ice ball&rdquo; (<strong>Figure 14</strong>). Tissue temperature is coldest adjacent to the probe, reaching -140&deg;C to -160&deg;C, and increases as distance from the probe increases. The visible rim of the ice ball represents the 0&deg;C isotherm, which is not tissue lethal. The lethal isotherm is not visible. It is typically located at least 5 mm central to the outer edge, with lethal temperatures -20&deg;C to -40&deg;C depending on tissue type.<sup>23</sup> For effective treatment, the lethal zone must cover the entire target lesion with at least a 5-mm ablation margin. The diameter of the &ldquo;ice ball&rdquo; is determined by the flow of gas and the length of the &ldquo;ice ball&rdquo; is determined by uninsulated probe length. If necessary, multiple probes can be utilized to increase the lethal zone. Precaution must be taken to ensure that the &ldquo;ice ball&rdquo; does not extend to involve other structures. One trial for cryoablation of breast cancer required that the mass was &gt; 5 mm deep to the skin and nipple.<sup>24</sup> However, in practice, there is no official criteria defining an acceptable distance from other structures. Techniques, such as injecting saline to create a buffer between the mass/treatment area and skin, can help prevent unintended damage.</p>
<p>The cryoablation procedure consists of a freeze-thaw-freeze cycle and can take up to 25 minutes depending on tumor size. This cycle destroys tumor cells through direct cell damage and death, vascular injury and ischemia, and indirect immunologic mechanisms.<sup>25</sup> During freezing, there is formation of intracellular, extracellular, and intravascular ice. Intracellular ice causes pore formation in the cell wall. Extracellular ice decreases extracellular free water and increases extracellular osmolarity. As a result, water exits the intracellular compartment causing cell shrinkage and dehydration.</p>
<p>During thawing, extracellular ice melts before intracellular ice causing increased free extracellular water. Endothelial damage caused by intravascular ice increases vascular permeability and contributes to increased extracellular water and decreased extracellular osmolarity. Osmotic gradients force water inside cells during thawing, causing cells to swell and burst leading to cell damage and death.<sup>25</sup> Delayed immune response then leads to absorption of damaged tissue, taking up to one year for the fibroadenoma and treatment zone to become nonpalpable. There is no routine follow-up imaging required for patients after cryoablation of fibroadenoma. Patients are followed clinically with a focus on palpability of the fibroadenoma and treatment zone.</p>
<p>Multiple studies have assessed outcomes of cryoablation for fibroadenomas. For example, Littrup et al found that 89% of all fibroadenomas, independent of original size were nonpalpable at 12 months.<sup>26</sup> Kaufman et al in 2004 found that 75% of all fibroadenomas were nonpalpable at one year with a 92% patient satisfaction rate.<sup>27</sup> In 2005, Kaufman et al demonstrated that 84% of previously palpable fibroadenomas and 94% of fibroadenomas &le; 2 cm were nonpalpable at an average follow-up time of 2.6 years with a 97% patient satisfaction rate.<sup>28</sup> They also showed a 99% median volume reduction of treatment zone by ultrasound in that follow-up interval.<sup>28</sup> Hahn et al showed that the average volume of the ablation zone was reduced by 75% at the one-year mark with a patient satisfaction rate of 96%.<sup>29</sup> Another study by Golatta et al assesses outcomes of cryoablation in fibroadenomas <u>&lt; </u>3 cm and found that 93% were nonpalpable at one year with a patient satisfaction rate of 97%.<sup>30</sup> Reported adverse events in these studies were minor, including localized skin changes, induration, hematoma, and continued breast pain.<sup>31, 32</sup></p>
<p><strong><i>Radiofrequency Ablation (RFA)&mdash;</i></strong>RFA utilizes a high-frequency alternating electric current administered via a probe centered in the target lesion, similar to cryoablation. The electric current heats adjacent tissue water molecules causing coagulation. Water molecules are more prevalent in neoplastic tissue compared to healthy surrounding tissue.<sup>32</sup> Furthermore, neoplastic vessels are abnormal and more susceptible to the coagulative effects as compared to healthy vasculature. These characteristics combine to cause preferential ablation of abnormal tissue. In RFA, a 1-cm margin of tissue is required around the lesion, limiting its use for lesions near the skin, chest wall, or breast implants.<sup>32</sup> Most literature regarding RFA centers around breast carcinoma and many consider it the most promising ablation modality for breast cancer with good long-term outcomes.<sup>33</sup> Studies investigating RFA for fibroadenoma are limited.<sup>32</sup> However, small studies have shown success. Teh et al reported on RFA treatment of 2 patients with fibroadenoma, both of whom had complete clinical and technical success at 6-month follow-up.<sup>34</sup> Further investigation to better delineate the role of RFA in fibroadenoma treatment is required.</p>
<p><strong><i>Laser Ablation&mdash;</i></strong>In laser ablation a thin fiber is inserted percutaneously under either ultrasound or MRI guidance. Low-power laser light energy is delivered via the fiber, which heats the surrounding tissues. Tumor necrosis depends on exposure time and tissue temperature.<sup>31</sup> Tissue temperatures can be followed by MR thermometry or with internal temperature monitors.<sup>32</sup> The area and shape of the necrosis is difficult to predict due to biologic variability, fiber tip charring, and changing optical and thermal properties of the tissue during laser photocoagulation.<sup>31</sup> Only a few studies have used this technique for fibroadenoma treatment. While this technique boasts quick treatment times and success rates comparable to fibroadenoma cryoablation in the few studies performed, there were more frequent complications, notably skin breakdown and pain.<sup>31</sup> As a result, it is not widely implemented in clinical practice.</p>
<p><strong><i>High-Intensity Focused Ultra-sonography (HIFU)&mdash;</i></strong>This is a relatively new, completely noninvasive ablative technique in which an ultrasound beam generated by a piezoelectric transducer is focused on the target tissue under either MRI guidance (MRgFUS) or ultrasound guidance.<sup>31,32</sup> The ultrasound beam propagates through tissue as a high-energy pressure wave that heats target tissue to 60-95&deg;C causing protein denaturation and coagulative necrosis without impacting surrounding healthy tissue.<sup>31</sup> This technique has shown success in breast cancer treatment, and phase II clinical trials are ongoing.<sup>32</sup> HIFU is also being investigated as a treatment for fibroadenoma. Hynynen et al treated 11 fibroadenomas with MRgFUS and had technical success of 72%, defined as partial or complete nonenhancement on follow-up MRI.<sup>35</sup> An additional study by Kovatcheva et al showed a volume reduction of 72.5% at a 12-month follow-up.<sup>36</sup> Other studies are ongoing with further patient follow-up required. While promising, more research into applications of this technique for fibroadenoma is necessary.</p>
<h2>Conclusion</h2>
<p>Fibroadenomas are common breast masses, especially in women under age 30. The imaging features of fibroadenoma overlap with multiple other benign and malignant breast masses. As such, fibroadenomas account for a large proportion of breast biopsies. Cosmesis is a central concern when treating fibroadenomas given the benignity and patient population. Open surgical excision remains the most common treatment choice. However, multiple minimally invasive techniques, notably ultrasound-guided percutaneous cryoablation, have been utilized to effectively treat fibroadenoma with improved cosmetic outcomes as well as other advantages including cost effectiveness, lack of general anesthesia risks, and increased patient comfort.</p>
<h2>References</h2>
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</ol>9723Overview of Parotid Gland Masses2018-10-16T12:10:58-04:002018-10-16T12:10:58-04:00Andrew Teh, D.O., Aswin Kumar, D.O., Claire Teh, OMS II, Lea Alhilali, M.D.<p>Of the major salivary glands, the parotid gland has the highest rate of tumor association, accounting for 64% to 80% of primary epithelial salivary gland tumors. Most parotid tumors are benign with malignancy only comprising approximately 15% to 32%.<sup>1</sup> The typical clinical presentation is a painless mass or swelling in the cheek about the mandibular rami. Facial nerve involvement generally suggests a malignant tumor, which may present with pain or paralysis. Imaging studies provide insight on the degree of glandular involvement, the nature of the tumor, and potential spread, and serve as an important baseline for therapeutic interventions. Familiarity with the normal anatomy of the parotid gland, as well as the imaging characteristics of common neoplasms involving the parotid gland, is crucial in establishing appropriate differential diagnoses and guiding clinical management.</p>
<h2>Benign</h2>
<h3>Pleomorphic Adenoma/Benign Mixed Tumor</h3>
<p>Pleomorphic adenomas, commonly referred to as benign mixed tumors (BMTs), are the most common benign salivary gland tumors (70% to 80%). Initially presenting as a slow-growing, painless cheek mass, these neoplasms typically appear in middle-aged females 30 to 60 years old.<sup>2-3 </sup>They are mixed tumors comprised of epithelial and myoepithelial cells.</p>
<p>On US, the appearance of BMT is a homogeneous hypoechoic, well-circumscribed mass. A nuclear medicine (NM) pertechnetate scan shows a photopenic/cold defect, differentiating them from a Warthin tumor (typically hot), but the appearance is indistinguishable from malignant parotid lesions (usually cold).<sup>4</sup> CT will demonstrate a well-circumscribed, homogeneously enhancing ovoid mass. Larger BMTs can show some heterogeneity to their enhancement pattern and may even present with central necrosis or dystrophic calcifications.<sup>5 </sup>T1 MRI sequences show a homogeneous hypointense mass, with larger BMTs showing hyperintense foci in cases of intratumoral hemorrhage. T2-weighted sequences will show uniform intermediate to high signal (<strong>Figure 1</strong>); very high T2 intensity greater than cerebrospinal fluid is fairly specific for BMTs. Diffusion-weighted imaging (DWI) usually shows higher apparent diffusion coefficient (ADC) signal compared to other parotid tumors, but this is not accurate enough to preclude biopsy. Contrast studies vary, ranging from mild to moderate enhancement (<strong>Figure 2</strong>).</p>
<p>Although benign, up to 15% of untreated pleomorphic adenomas can undergo malignant transformation, known as carcinoma ex pleomorphic adenoma. Characteristics include rapid growth over the course of a few months and pain.<sup>1 </sup>For both conditions, surgical excision remains the gold standard, although recurrence is common if the tumor extends past its capsule. A partial or total parotidectomy has been found to dramatically decrease recurrence rates compared to lesional excision.<sup>6</sup></p>
<h3>Warthin Tumors</h3>
<p>Warthin tumors<strong> </strong>are the second most common benign salivary gland tumor, accounting for 10% of parotid tumors. They present with painless swelling, with 20% of lesions appearing multifocal (unilateral or bilateral). Warthin tumors are classically seen in elderly men in the 6th decade of life, with a strong association with smoking and radiation exposure.<sup>1,7 </sup>Warthin tumors have also been termed lymphomatous papillary cystadenoma, corresponding with their histological characteristics: glandular structures with papillary cystic arrangement, along with a stroma filled with lymphoid tissue.<sup>1</sup></p>
<p>Contrast-enhanced CT shows a smoothly marginated, ovoid mass occasionally located in the tail (posterior portion) of the superficial lobe of the parotid gland (<strong>Figure 3</strong>). Cystic components can be seen in up to 30% of lesions and may be difficult to differentiate from a cystic lymph node, branchial cleft cyst, or other cystic mass. Presence of a mural nodule may also be suggestive of a Warthin tumor.<sup>8</sup> T1 MRI sequences typically show low signal in the solid and cystic components, although the presence of proteinaceous debris or hemorrhage may increase the T1 signal. Solid components show minimal enhancement (<strong>Figure 4</strong>). On US, Warthin tumors will show well-defined anechoic areas toward the tail of the superficial parotid gland reflecting cystic components.<sup>5,8,9</sup></p>
<p>The incidence of malignancy is &lt;1%. Management involves either surgical excision or routine monitoring, which can be advantageous to avoid iatrogenic complications.<sup>7</sup> Local recurrence is exceedingly rare but more likely in multifocal disease.</p>
<h3>Facial Nerve Schwannoma</h3>
<p>Facial nerve schwannomas (FNSs)<strong> </strong>are rare benign neoplasms arising from Schwann cells along cranial nerve (CN) VII, the facial nerve. In the parotid parenchyma, they may present similarly to pleomorphic adenomas as a painless and slow-growing mass. Uncommonly, they present with facial weakness or paralysis. Multiple schwannomas have an association with neurofibromatosis type 2 (NF-2).</p>
<p>Imaging findings of FNS on contrast-enhanced CT are a round or oval well-circumscribed enhancing intraparotid mass. Proximal lesions may cause enlargement of the stylomastoid foramen. MRI shows a well-defined mass that is T1 isointense and T2 slightly hyperintense to muscle with enhancement on postgadolinium images (<strong>Figure 5</strong>). Larger lesions may have a characteristic intramural cyst.<sup>8,10-11</sup></p>
<p>Preoperative diagnosis of FNS is extremely difficult and uncommon. Diagnosis is often made intraoperatively via electrical stimulation and tissue biopsy, followed by radiographic staging to determine neoplastic extent.<sup>10,12 </sup>Total resection is curative; however, this may be declined if the nerve cannot be salvaged.</p>
<h3>Benign Lymphoepithelial Lesions (BLELs)</h3>
<p>Benign lymphoepithelial lesions (BLELs)<strong> </strong>are relatively common in HIV patients and are sometimes concurrent manifestations of Sj&ouml;gren syndrome.<sup>13,14 </sup>Both parotid glands are often involved and can range from purely cystic lesions to mixed cystic and solid masses. They occur more frequently in women than men (3:1), and within the 4<sup>th</sup> to 7<sup>th</sup> decades of life. Similar to other benign parotid masses, these typically present as painless swelling with enlargement of the parotid glands.<sup>15</sup></p>
<p>Imaging features overlap with Warthin tumors of the parotid and show bilateral cystic and solid masses within enlarged parotid glands (<strong>Figure 6</strong>). US shows the cystic components to be anechoic with variable posterior acoustic enhancement. Solid components are predominantly hypoechoic in appearance, with identified intraparotid lymph nodes showing prominent cortex and hilar architecture. CT will show bilateral solid and cystic masses involving the parotid glands. Postcontrast images show thin rim enhancement of the cystic components and heterogeneous enhancement of the solid components. MRI sequences show hypointense T1 and hyperintense T2 signal in cystic components with variable enhancement of the solid components. Waldeyer&rsquo;s lymphatic ring is typically enlarged with high T2 signal and can suggest BLEL in an HIV patient.<sup>8,11,15</sup></p>
<p>Histology shows lymphocytic infiltration with lymphocytes and germinal center hyperplasia, resulting in atrophy of the parotid parenchyma. Malignant transformation is rare and can arise from the epithelial or lymphoid component, known as lymphoepithelial carcinomas (LEC). BLEL may be monitored, whereas LEC should be excised along with lymph node dissection or with radiation therapy.<sup>15</sup></p>
<h2>Malignant</h2>
<h3>Mucoepidermoid Carcinoma</h3>
<p>Mucoepidermoid carcinoma<strong> </strong>is the most common primary malignant tumor of the parotid gland. Initial presentation is a palpable parotid mass. Additional symptoms may include pain, facial nerve paralysis, or sensory deficits in the V3 distribution. These tumors typically affect adults ages 35 to 65 years but can also occur in children. Histology consists of epidermoid and mucous-secreting cells. Treatment depends on the grade of tumor, with local resection sufficient for low-grade tumors, but wide surgical excision and radiotherapy required for high-grade lesions.<sup>16-17</sup></p>
<p>Imaging characteristics may vary based on the histologic grade of the tumor. Low-grade lesions can present as a well-circumscribed parotid mass, mimicking benign entities, while high-grade lesions can have ill-defined or infiltrative margins (<strong>Figure 7</strong>). Evaluation for malignant nodes or perineural spread along CN VII is important for accurate staging (<strong>Figure 8</strong>). Loss of the normal fat in the stylomastoid foramen, abnormal enhancement in the mastoid segment of CN VII, or osseous involvement of the mandible or skull base indicates a higher-grade malignancy and delineates the extent of disease.<sup>8</sup></p>
<p>Contrast-enhanced CT will typically show an enhancing soft-tissue mass in the parotid gland. Cystic changes can be seen due to mucous-producing cells. On MRI, the lesion will have heterogeneous T1 and T2 signal with areas of high T2 signal indicating cystic changes. Indistinct margins suggest a higher-grade tumor. DWI may show restricted diffusion and/or low ADC signal, but is nonspecific, as a Warthin tumor may show similar findings.<sup>8</sup> Enhancement is typically heterogeneous, with cystic components having little enhancement.<sup>8,11</sup></p>
<p>Recurrence rate correlates with higher histologic grade. Lower-grade tumors have been reported to have up to a 90% 10-year survival rate. Evidence of metastatic spread or infiltrative margins portends a poorer prognosis and increased rate of recurrence. Late recurrence is possible and routine monitoring for up to 10 years is recommended <sup>8,16-17</sup></p>
<h3>Adenoid Cystic Carcinoma</h3>
<p>Adenoid cystic carcinoma (ACC) is the second most common primary malignancy of the parotid gland. The lesion presents as a slow-growing parotid mass with pain reported in up to one-third of cases. Peak incidence is between the 5th and 7th decades, and it is rarely seen before age 20. Among all head and neck tumors, ACC has the highest propensity for perineural spread.<sup>18</sup></p>
<p>Imaging characteristics include an enhancing parotid mass with either well-circumscribed borders or infiltrative margins depending on the histologic grade. Enhancement on CT or MR is typically homogenous with T1- and T2-weighted images showing variable low to intermediate signal intensity (<strong>Figure 9</strong>). DWI may show restricted diffusion but is nonspecific in differentiating ACC from a benign Warthin tumor.<sup>8</sup> As with all parotid masses, but especially ACC, close attention should be paid to potential perineural spread.<sup>8,11</sup></p>
<p>ACC typically has a good short-term prognosis but poor long-term prognosis. Late recurrence can occur up to 20 years after diagnosis. Treatment is typically surgical resection with postoperative radiotherapy. Metastatic involvement of the lungs and bones is more common compared with lymph node spread.<sup>8,18</sup></p>
<h3>Lymphoma</h3>
<p>Lymphoma of the parotid glands is of the non-Hodgkin lymphoma (NHL) variety with three distinct forms: primary nodal, systemic, or primary parenchymal. Initial presentation is of a painless, enlarging parotid mass with cervical lymphadenopathy. Mean age of presentation is 55 years with a 1.5:1 male-to-female predominance.<sup>19 </sup></p>
<p>Imaging characteristics of parotid NHL depend on the type. Nodal NHL usually presents as a well-circumscribed lesion, while the parenchymal type can have infiltrative or indistinct margins. Contrast-enhanced CT shows mild to moderate enhancement and frequent periparotid or upper cervical lymphadenopathy. MRI may show an intermediate T1 signal intensity mass within a background of hypointense parotid gland. Post-gadolinium administration shows mild to moderate enhancement (<strong>Figure 10</strong>). F-18 fluorodeoxyglucose (FDG) PET/CT will show avid activity in nodal NHL.<sup>11</sup></p>
<p>NHL of the parotid has an increased incidence with autoimmune disorders or immunosuppression and is frequently associated with Sj&ouml;gren syndrome, rheumatoid arthritis, or systemic lupus erythematosus. Treatment is typically with chemotherapy and radiation.<sup>1,8,19</sup></p>
<h3>Metastases</h3>
<p>Metastases<strong> </strong>should be a consideration for parotid lesions in patients with a known malignancy, especially head and neck malignancy, such as squamous cell carcinoma. Skin lesions involving the face and scalp, such as squamous cell carcinoma or melanoma, account for the majority of parotid metastases. Systemic metastases to the parotid gland are extremely rare, usually originating from lung or breast cancers.</p>
<p>Imaging findings include one or more intraparotid masses. Cervical lymphadenopathy may also be present. Lesions can be well circumscribed or have indistinct margins. Enhancement pattern is typically homogenous, although if necrosis is present, there may be central areas of decreased enhancement. MR is the best modality for determining perineural spread, and FDG PET/CT can be helpful in assessing involvement of small extra parotid nodes and other sites of metastatic disease.<sup>8,11</sup></p>
<h2>Summary</h2>
<p>&gt;Parotid masses have a variety of etiologies that range from benign to malignant. Although many lesions have some overlapping features, imaging appearance and patient demographics often aid in narrowing the list of differential considerations. Familiarity of the imaging characteristics of common parotid masses is critical in providing a comprehensive evaluation that includes determining lesion etiology, assessing staging for malignant lesions, and guiding overall management.</p>
<h2>References</h2>
<ol>
<li>Eveson JW, Auclair P, Gnepp DR, et al. Tumours of the salivary glands. In: Barnes L, Eveson JW, Reichart P, Sidransky D, eds. Pathology and genetics of head and neck tumours, 1<sup>st</sup> ed. Lyon, France: IARC Publications; 2005:212-213,242-243.</li>
<li>Som PM, Shugar JM, Sacher M, et al. Benign and malignant parotid pleomorphic adenomas: CT and MR studies. J Comput Assist Tomogr 1988;12(1):65-69.</li>
<li>Thoeny HC. Imaging of salivary gland tumours. Cancer Imaging 2007;7(1):52-62.</li>
<li>Kulkarni M, Shetkar S, Joshi P, et al. Incidental Warthin tumor on pertechnetate scintigraphy. Clin Nucl Med 2016;41(9):728-729.</li>
<li>Yerli H, Aydin E, Coskun M, et al. Dynamic multislice computed tomography findings for parotid gland tumors. Comput Assist Tomogr 2007;31(2):309-316.</li>
<li>Moonis G, Patel P, Koshkareva Y, et al. Imaging characteristics of recurrent pleomorphic adenoma of the parotid gland. Am J Neuroradiol 2007;28(8):1532-1536.</li>
<li>Espinoza S, Felter A, Malinvaud D, et al. Warthin&rsquo;s tumor of parotid gland: surgery or follow-up? Diagnostic value of a decisional algorithm with functional MRI. Diagn Interv Imaging 2016;97(1):37-43.</li>
<li>Abdullah A, Rivas FR, Srinivasan A. Imaging of the salivary glands. Semin Roentgenol 2013;48(1):65-74.</li>
<li>Yabuuchi H, Matsuo Y, Kamitani T, et al. Parotid gland tumors: can addition of diffusion-weighted MR imaging to dynamic contrast-enhanced MR imaging improve diagnostic accuracy in characterization? Radiol 2008;249(3):909-916.</li>
<li>Damar M, Dinc AE, Elicora SS, et al. Facial nerve schwannoma of parotid gland: difficulties in diagnosis and management. Case Rep Otolaryngol 2016;2016,1-4.</li>
<li>Lee YY, Wong KT, King AD, et al. Imaging of salivary gland tumours. Eur J Radiol 2008;66(3):419-436.</li>
<li>Caughey RJ, May M, Schaitkin BM. Intraparotid facial nerve schwannoma: diagnosis and management. Otolaryngol Head Neck Surg 2004;130(5):586-592.</li>
<li>Martinoli C, Pretolesi F, Del bono V, et al. Benign lymphoepithelial parotid lesions in HIV-positive patients: spectrum of findings at gray-scale and Doppler sonography. Am J Roentgenol 1995;165(4):975-979.</li>
<li>Jeong HS, Lee HK, Ha YJ, et al. Benign lymphoepithelial lesion of parotid gland and secondary amyloidosis as concurrent manifestations in Sj&ouml;gren syndrome. Arch Plast Surg 2015;42(3):380-383.</li>
<li>Schneider M, Rizzardi C. Lymphoepithelial carcinoma of the parotid glands and its relationship with benign lymphoepithelial lesions. Arch Pathol Lab Med 2008;132(2):278-282.</li>
<li>Yadav R, Battoo AJ, Mir AW, et al. Bulbar conjunctival metastasis from mucoepidermoid carcinoma of parotid&mdash;a case report and review of literature. World J Surg Oncol 2017;15(1):10.</li>
<li>Lewis AG, Tong T, Maghami E. Diagnosis and management of malignant salivary gland tumors of the parotid gland. Otolaryngol Clin North Am 2016;49(2):343-380.</li>
<li>Ko JJ, Siever JE, Hao D, et al. Adenoid cystic carcinoma of head and neck: clinical predictors of outcome from a Canadian centre. Curr Oncol 2016;23(1):26-33.</li>
<li>Aydin S, Demir MG, Barisik NO, et al. Extranodal marginal zone lymphoma of the parotid gland. J Maxillofac Oral Surg 2016;15(Suppl 2):346-350.</li>
</ol>9721MRI Degenerative Disease of the Lumbar Spine: A Review2018-10-16T12:01:44-04:002018-10-16T12:01:44-04:00Mark Buller, MD<p>Low back pain is an exceedingly common problem, with a lifetime prevalence of 70% to 85%.<sup>1</sup> This condition is the most common cause of disability in people ages 45 years or younger, with an estimated economic impact of over $100 billion dollars per year, predominantly due to loss of productivity.<sup>2</sup> The etiology of low back pain is multifactorial and is influenced by genetics,<sup>3</sup> age,<sup>4-6</sup> sex<sup>4</sup> and mechanical stresses.<sup>4,7</sup></p>
<p>Imaging plays a critical role in the diagnosis of low back pain. MRI has become a mainstay in the workup of low back pain due to its excellent soft tissue contrast, cross-sectional capability, and lack of ionizing radiation. This paper will present common MRI findings associated with low back pain, as well as grading systems and common nomenclature to assist in consistent and reproducible reporting of these findings.</p>
<h2>MRI Imaging Techniques</h2>
<p>An MRI of the lumbar spine generally includes a sagittal T1-weighted spin echo sequence, a sagittal T2-weighted spin echo sequence, and axial T2-weighted images. Additional sequences including axial T1-weighted sequences, sagittal fat-nulling T2-weighted sequences such as short tau inversion recovery (STIR) or modified Dixon (mDixon), and gadolinium-based contrast enhanced T1-weighted sequences may be obtained depending on the institution and the indication for the MRI examination.</p>
<p>Sagittal T1-weighted images are useful in the assessment of bone marrow, which is normally fatty in adults and demonstrates high T1 and T2 signal. Alignment of the vertebral bodies can also be assessed on the sagittal T1-weighted sequence. Due to the high contrast between fat and nerve roots, the T1 sagittal sequences are excellent for assessing the degree of neural foraminal stenosis.</p>
<p>Sagittal T2-weighted images provide excellent contrast between cerebrospinal fluid (CSF) in the thecal sac and the surrounding structures, allowing for assessment of the degree of spinal stenosis at multiple levels on a single image. These sequences are also useful for assessment of the intervertebral discs, and the presence of disc herniation. Fluid sensitive sequences such as STIR and mDixon are used for detecting areas of bone marrow edema.</p>
<p>Axial T2-weighted images provide a level-by-level assessment of the relationship between the thecal sac and the surrounding bony and ligamentous structures and are particularly useful for assessing spinal stenosis and narrowing of the lateral or subarticular recesses. These sequences are also used in assessing the facet joints and ligamentum flava.</p>
<p>In addition to the previously mentioned techniques, several other MRI sequences can be used for assessment of the lumbar spine. There is evidence to suggest that upright MRI of the lumbar spine provides a more accurate assessment of the physiology of low back pain as many patients are more symptomatic when standing.<sup>8,9</sup> However, limited availability, high false-positive rates, and increased motion artifact have limited widespread adoption of this technique.<sup>8</sup> Other techniques such as T1 and T2 relaxation mapping and new sequences like sodium MRI, magic echo and T1<sub>&rho;</sub><sub> </sub>are being developed to assess early molecular changes in the intervertebral disc.<sup>10</sup></p>
<h2>Normal Anatomy</h2>
<h3>Vertebral Bodies</h3>
<p>Lumbar vertebrae are composed of a vertebral body anteriorly, which gives rise to bilateral pedicles from its superior aspect. These extend posteriorly and connect to the transverse processes, which project laterally, and the lamina, which project posteromedially. The lamina come together in the midline and connect to the posteriorly projected spinous process. Interposed between each pedicle and lamina are the superior and inferior articular processes, joined by the pars interarticularis.</p>
<p>The vertebral bodies consist of an outer layer of cortical bone, which is low signal intensity on T1- and T2-weighted imaging and surrounds the inner trabecular bone. Trabecular bone is normally high signal on T1- and T2-weighted sequences in adults due to its fatty marrow.</p>
<p>The posterior wall of the vertebral body and inner margins of the pedicles and lamina form a bony ring around the thecal sac. The neural foramina are bordered superiorly and inferiorly by the pedicles of adjacent vertebral bodies, anteriorly by the posterolateral margin of the suprajacent vertebral body and intervertebral disc, and posteriorly by the superior articular process of the subjacent vertebral body. Neural foramina allow the passage of lumbar nerve roots from the thecal sac to the peripheral tissues. Nerve roots within the neural foramina are low signal on T1- and T2-weighted imaging and are normally surrounded by a rim of perineural fat.</p>
<h2>Intervertebral Discs</h2>
<p>Interposed between the vertebral bodies are the intervertebral discs (<strong>Figure 1</strong>). These discs form the anterior articulation of the vertebral column and have two components: the outer annulus fibrosis (AF) and the inner nucleus pulposis (NP). The AF is a dense fibrocartilaginous structure comprised of 15 to 20 layers of obliquely oriented fibers that run from the inferior endplate of the suprajacent vertebral body to the superior endplate of the subjacent vertebral body.<sup>11</sup> These fibers are primarily comprised of type 1 collagen.<sup>12</sup> This portion of the intervertebral disc normally demonstrates low T1 and low T2 signal. The NP is composed of a loose type 2 collagen matrix and is 70% to 90% water and proteoglycans.<sup>12</sup> The NP demonstrates high T2 and low T1 signal, due to its high water content. A low T2 signal band can be seen centrally within the NP in patients over age 30 and represents a fibrous band or cleft.<sup>13</sup> These discs contact the vertebral body endplates, which are made up of hyaline cartilage on the vertebral body side and fibrocartilage along the disc.<sup>11</sup></p>
<h3>Facet Joints</h3>
<p>The posterior articulation of the vertebral bodies is formed by the facet (zygoapophyseal) joints. These are obliquely oriented synovial joints comprised anterolaterally of the superior articular process of the subjacent vertebral body and posteromedially by the inferior articular process of the suprajacent vertebral body. Facet joints have articular surfaces composed of hyaline cartilage within a fibrous joint capsule lined with synovium.<sup>11</sup> The joint spaces of the facet joints normally measure 2 to 4 mm and demonstrate isointense to high T2 signal.<sup>14</sup></p>
<h3>Ligamentum Flava</h3>
<p>Multiple ligamentous structures contribute to the stability of the spinal column. These include the anterior longitudinal ligament, the posterior longitudinal ligament, the interspinous ligament, and the supraspinous ligament. Of particular interest when considering degenerative disease of the lumbar spine are the ligamentum flava, paired ligaments that extend between the lamina of adjacent vertebral bodies. These ligaments are normally thin and low signal on T1- and T2- weighted sequences.</p>
<h2>Degenerative Disease</h2>
<h3>Intervertebral discs</h3>
<p>Normal intervertebral discs transition through three phases: growth, maturation, and degeneration.<sup>15</sup> The growth phase is characterized by synthesis of aggrecan and procollagens and increased type 2 collagen and takes place between ages 0 and 15. The maturation phase occurs with a reduction in the synthesis and volume of type 2 collagen in the NP from approximately 15 to 40 years of age. The final stage is degeneration, characterized by increased fibrosis with decreasing type 2 collagen and increasing type 1 collagen, which takes place after age 40.</p>
<p>This disc degeneration, as well as annular fissures and apophyseal osteophyte formation, in the absence of disc height loss, have been termed spondylosis deformans and are considered normal processes associated with aging.<sup>16-18</sup> On MRI, apophyseal osteophytes are characterized by low T1 and T2 outgrowths along the anterior and lateral margins of the endplates. Disc degeneration manifests as loss of T2 signal in the NP. Annular fissures are small areas of T2 hyperintensity in the posterior AF. More extreme changes, including severe disc fissuring, disc height loss and endplate erosion, have been termed intervertebral osteochondrosis, which is a pathologic process.<sup>16-18</sup></p>
<p>Pfirrmann et al proposed a grading system for intervertebral disc degeneration based on disc structure, distinction between the NP and AF, NP signal intensity and disc height (<strong>Table 1</strong>).<sup>19</sup> This grading system demonstrated good interobserver reliability. A review of the literature in 2005 by Kettler et al found that the Pfirrmann grading system was the only MRI-based system for disc degeneration with a kappa value of greater than 0.6.<sup>20</sup> This system has since been modified by Griffith et al to increase the discriminatory power in the elderly population, with three additional severity levels and a quantitative measurement of disc height reduction.<sup>21</sup></p>
<p>Annular fissures are regions of high T2 signal intensity seen in the posterior AF of degenerated discs (<strong>Figure 2</strong>). Nearly all degenerated discs have annular fissures, although these may not be visible on MRI.<sup>22</sup> The role of annular fissures in pain generation is uncertain, with multiple studies noting that annular fissures are often seen in asymptomatic individuals.<sup>23-26</sup> Additionally, evidence suggests that the presence of annular fissures does not increase progression of degenerative disc disease when compared to discs without fissures.<sup>27</sup> For these reasons, the Combined Task Force (CTF) of the North American Spine Society, American Society of Spine Radiology and American Society of Neuroradiology recommend the term &ldquo;annular fissure&rdquo; instead of &ldquo;annular tear&rdquo; to avoid implying that these regions of signal intensity are a type of acute disc injury.<sup>28</sup></p>
<p>Another common disc-related finding in degenerative disease of the lumbar spine is disc herniation. There are multiple systems for classification of disc herniations; however, the two most studied systems are those proposed by Jensen et al<sup>29</sup> and Fardon et al.<sup>28</sup> The Jensen classification system splits disc herniations into three categories: disc bulges, protrusions and extrusions. Bulges are defined as symmetric extensions of disc material beyond the interspace. Protrusions are focal or asymmetric extensions of disc material beyond the interspace with the base of the herniation being wider than the apex. Finally, extrusions are defined as more extreme extensions of disc material beyond the interspace with the dimension of the extruded component either wider than the base or not connected to the base. The findings of the CTF published by Fardon et al do not consider disc bulges a form of herniation as bulging can be a normal variant or the result of adjacent bony remodeling or ligamentous laxity.<sup>28</sup> The CTF defines protrusions and extrusions as involving less than 25% of the circumference of the disc, in addition to the features described by Jensen et al (<strong>Figure 3</strong>). Additional terminology proposed by the CTF includes &ldquo;sequestration&rdquo; as a subset of extrusion where the extruded material is not continuous with the parent disc (<strong>Figure 4</strong>). A recent systematic review of the literature found that the recommendations by the CTF demonstrated superior interrater reliability compared to Jensen et al.<sup>30</sup> The CTF recommends that this classification be coupled with the localization system proposed by Wiltse et al,<sup>31</sup> which divides the spinal canal into central, subarticular, foraminal and extraforaminal zones (<strong>Figure 5</strong>).</p>
<p>An alternate method for classification of disc herniations differentiates subligamentous herniations from extra-ligamentous herniations. This classification scheme, proposed by Oh et al,<sup>32</sup> describes five criteria that can be used to determine extra-ligamentous herniations: spinal canal compromise of more than half its dimension, internal signal difference in the herniated disc, ill-defined margin of the herniation, disruption of low-signal intensity line covering the herniation, and the presence of an internal dark line in the herniated disc. The authors note that this type of classification is potentially more clinically useful as minimally invasive methods are more successful with subligamentous disc herniations than extra-ligamentous herniations.</p>
<p>Another clinically oriented classification scheme was developed at Michigan State University by Mysliwiec et al.<sup>33</sup> This grading system proposes to separate disc herniations into those that are &ldquo;substantial&rdquo; and require surgical intervention, and those that are not and are more likely to have poor surgical outcomes. The authors propose using a line drawn between the anterior margins of the facet joints in the axial plane as a reference for the extent of disc herniation. Those herniations that do not extend more than 50% of the distance between the interspace and intrafacet line are classified grade 1 and should be managed conservatively. Those extending beyond grade 1 but not beyond the intrafacet line (grade 2), and those extending beyond the intrafacet line (grade 3) were treated surgically, with good outcome rates that compared favorably to existing literature. While this technique is less subjective than other schemes, it is somewhat limited in that it cannot be used in patients with abnormal facet joints and ligamentum flavum hypertrophy.</p>
<h3>Vertebral Body Endplates</h3>
<p>Degenerative endplate changes have been classified by Modic et al,<sup>34,35</sup> into three categories: Type 1 changes are edematous changes related to subchondral end plate fractures, formation of vascularized fibrous tissue and an acute reparative response. On MRI, these changes are characterized by increased T2 and decreased T1 signal in the bone marrow adjacent to the endplate. Type 2 changes are related to fatty replacement of normal marrow and are more chronic and stable. These changes will demonstrate increased T1 and T2 signal, with loss of signal on fat suppression sequences. Type 3 changes relate to chronic endplate sclerosis and development of dense woven bone. This dense bone is low signal intensity on both T1- and T2-weighted sequences. Transitions through these stages are not uniformly progressive, and multiple studies have shown resolution of Type 1 changes or progression from Type 2 change to Type 1 change.<sup>35-37</sup> Type 1 and Type 3 changes are more associated with low back pain and instability, while Type 2 change is more frequently seen in degenerative disc disease and is less associated with back pain.<sup>38</sup> The Modic classification system has been shown to have good interrater reliability.<sup>39</sup></p>
<p>More recently, a classification system for endplate changes based on morphology was proposed by Rajasekaran et al.<sup>40</sup> This system grades defects in the endplate, with severity based on the area of the endplate involved. The authors demonstrated good correlation between increasing stage of endplate destruction and increasing degeneration of the associated disc.</p>
<h3>Facet Joints</h3>
<p>Degenerative changes can occur in the facet joints independent of the presence of degenerative disc disease.<sup>41</sup> Findings of degenerative disease in the facet joints include joint space narrowing, subchondral erosions and cystic change, osteophyte formation, and synovial cyst formation (<strong>Figure 6</strong>). Weishaupt et al utilized these features to develop a grading system for facet disease on MRI.<sup>13</sup> (<strong>Table 2</strong>). This system was found to have moderate to good agreement with CT grading of facet disease, and excellent agreement when allowing for differences of only one grade. This was the only system for MR facet joint degeneration grading recommended by Kettler et al following their literature review.<sup>20 </sup></p>
<p>Superimposed on independent degeneration of the facet joints, loss of disc height can produce a cascade of events causing increased degeneration of the facet joints and surrounding structures. Loss of height causes abnormal contact of the superior tip of the superior articular process of the subjacent vertebra with the undersurface of the pedicle of the suprajacent vertebra. Additional abnormal contact forms between the inferior tip of the inferior articular process of the suprajacent vertebra with the posterior surface of the pars interarticularis of the subjacent vertebra. These contact points cause additional degenerative remodelling, osteophyte formation, and neocyst/synovial cyst formation secondary to altered mechanical forces. These changes can lead to thinning and fractures of the pars interarticularis, neoarthroses of the superior articular facet/pedicle, and narrowing of the neural foramina. These changes are summarized and accompanied by detailed line diagrams in a review by Jinkins.<sup>42</sup></p>
<h3>Ligamentum Flava</h3>
<p>Ligamentum flavum thickening is a common finding in degenerative disease of the lumbar spine, manifested by increased thickness of low T1 and T2 signal along the posterolateral spinal canal (<strong>Figure 7</strong>). Debate remains about the etiology of the thickening of the ligamentum flava seen in degenerative spine disease. Some authors suggest that this is due to true hypertrophy of the ligament secondary to increased fibrotic change in response to adjacent inflammatory markers.<sup>43</sup> Others suggest that the thickening observed is not true hypertrophy, but rather buckling of a redundant ligament secondary to loss of disc height.<sup>42.44</sup></p>
<h2>Structural sequelae</h2>
<h3>Spinal Stenosis</h3>
<p>The previous section discussed the common degenerative findings affecting the ring of structures surrounding the thecal sac&mdash;at the endplates and discs anteriorly, the facet joints posterolaterally, and the ligamentum flava posteriorly. There is conflicting evidence regarding the clinical significance of these findings in isolation and uncertainty regarding which degenerative findings are associated with low back pain.<sup>5,45-47</sup> Indeed, a literature review by Brinjikji et al<sup>47</sup> found that the percentage of asymptomatic 80-year-old patients with disc degeneration, disc bulging and facet hypertrophy was 96%, 84%, and 83%, respectively. This uncertainty makes clinical correlation of back pain with imaging findings extremely difficult. However, these degenerative findings in combination often cause narrowing of the spinal canal and neural foramina with resultant compression of lumbar nerve roots. This compression results in radicular symptoms such as leg pain and weakness, which can be correlated with imaging findings of nerve compression.<sup>48,49</sup></p>
<p>As with disc herniation, there are multiple grading systems for nerve root compression in the spinal canal. Pfirrmann et al proposed a system to grade the effect of disc herniation on the lumbar nerve roots using three grades: contact of the nerve root, displacement of the nerve root (<strong>Figure 3A</strong>), and compression of the nerve root (<strong>Figure 4</strong>). This scale was found to have good interrater reliability and good correlation with surgical grading.<sup>50</sup></p>
<p>An alternate grading system was subsequently published by van Rijn et al, which used a 5-point scale that was subsequently dichotomized to either &ldquo;no root compression&rdquo; (for initial categories &ldquo;definitely no root compression,&rdquo; &ldquo;possibly no root compression&rdquo; and &ldquo;indeterminate&rdquo;) and &ldquo;root compression&rdquo; (for initial categories &ldquo;possibly root compression&rdquo; and &ldquo;definitely root compression&rdquo;).<sup>51</sup></p>
<p>A recent review of grading systems for lumbar disc herniations noted that while the van Rijn system was the most reliable grading system to date, the Pfirrmann system has been clinically correlated and demonstrates very good reliability at higher grades, allowing for accurate capture of symptomatic and clinically relevant lesions.<sup>52</sup></p>
<h3>Neural Foraminal Stenosis</h3>
<p>Classification systems for neural foraminal narrowing are based on the degree of effacement of perineural fat within the foramen on T1-weighted sagittal images (<strong>Figure 8</strong>). Two such systems were proposed by Wildermuth et al<sup>53</sup> and Lee et al.<sup>54</sup> Both systems use four grades that represent normal foramina and mild, moderate, and severe foraminal narrowing (<strong>Table 3</strong>).</p>
<p>The clinical correlation of the Wildermuth and Lee systems was compared by Park et al<sup>55</sup> who concluded that while both systems had similarly excellent interrater reliability, the Wildermuth grading scheme more precisely reflected clinical symptoms, particularly in patients over 50 years of age.</p>
<h2>Conclusion</h2>
<p>Degenerative disease of the lumbar spine is a common condition that radiologists will encounter frequently. MRI is a mainstay in the assessment of low back pain and degenerative disease of the lumbar spine. This paper has reviewed the common findings affecting the vertebral bodies, intervertebral discs, facet joints, and ligamentum flava, as well as the combined effects of these changes on the spinal canal and neural foramina. Multiple grading systems were presented, with supporting evidence, to help increase the accuracy and consistency when reporting these findings.</p>
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</ol>9697Shoulder Impingement and Associated MRI Findings2018-07-09T15:29:58-04:002018-07-09T15:29:58-04:00Cameron P. Smith, D.O., Christos E. Vassiliou, D.O., Jason R. Pack, M.D., Donald von Borstel, D.O.<p>Shoulder pain is a common musculoskeletal medical condition affecting 7% to 26% of individuals and is the third most common musculoskeletal-related complaint in the primary care setting.<sup>1,2</sup> Rotator cuff pathology is a common etiology for shoulder pain, with impingement of the rotator cuff often playing an important role. Rotator cuff impingement was first described by Neer et al when he stated that 95% of rotator cuff tears were attributed to impingement and generally occur in patients over age 40.<sup>3,4</sup> Two predominant types of shoulder impingement have been described: intrinsic and extrinsic.</p>
<p>Intrinsic shoulder impingement is relatively uncommon and seen almost exclusively with overhead throwing athletes.<sup>5</sup> It is a result of extreme abduction and external rotation, which can lead to entrapment of the supraspinatus and/or the infraspinatus tendons between the glenoid.<sup>6</sup> MRI appearance of intrinsic impingement is varied and includes labral and rotator cuff pathology. The infraspinatus tendon is commonly injured, especially in patients under age 30, with MRI findings ranging from undersurface tears to complete tears.<sup>6,7</sup></p>
<p>Extrinsic, or external, impingement is one of the more common causes of shoulder pain and a frequent source for an orthopedic evaluation.<sup>8</sup> Extrinsic shoulder impingement is most commonly related to mechanical compression from the acromion, acromioclavicular joint, and the coracoacromial ligament.<sup>3,9</sup> Numerous operative and nonoperative treatment options have been described for extrinsic impingement, ranging from physical therapy and injections to acromioplasty and Mumford procedures.</p>
<p>The purpose of this article is to help understand the relevant anatomy with regard to the subacromial region, review the imaging findings, and discuss the differing etiologies of extrinsic impingement. This knowledge will allow radiologists to effectively communicate with clinicians and help guide appropriate treatment.</p>
<h2>Anatomy</h2>
<p>The coracoacromial arch provides a safeguard for the shoulder, limiting superior migration of the humeral head. The coracoacromial arch is composed of (from anterior to posterior) the coracoid process, coracoacromial ligament, and the acromion process. Inferior to these structures, and coursing through the arch, are the subacromial/subdeltoid bursa, supraspinatus tendon, and biceps tendon. The humeral head provides the posterior/inferior border of the arch (Figure 1). Processes that decrease the space within the coracoacromial arch presumably may lead to impingement-like symptoms.</p>
<p>The <em>coracoid process</em> is a hook-like osseous structure arising from the superolateral edge of the scapula and extends in an anterolateral orientation. The coracoid is an anchor point for several ligaments and tendons, including the pectoralis minor, coracobrachialis, and short head of the biceps brachii tendons. Also, the coracoid is an attachment site for the coracohumeral, coracoacromial, coracoclavicular, and superior transverse ligaments.<sup>10</sup> The coracoid process can be palpated below and at the lateral edge of the clavicle. Known as the &ldquo;Surgeon&rsquo;s Lighthouse,&rdquo; the coracoid process serves as a landmark to avoid neurovascular injury, as major neurovascular structures traverse medially to the coracoid process.<sup>11</sup></p>
<p>The <em>coracoacromial ligament</em> is a thick triangular ligamentous structure extending inferomedially from the anterolateral undersurface of the acromion to the lateral border of the coracoid process. This structure provides an osseo-ligamentous static restraint to superior humeral head displacement. Ligamentous connection of the coracoacromial ligament and the rotator interval capsule is thought to prevent inferior migration of the glenohumeral joint.<sup>12</sup> Coracoacromial ligament thickness is normally 2 to 5.6 mm.<sup>13</sup> Implicated as a pain generator in impingement syndrome, treatment of the coracoacromial ligament has been controversial. There is uncertainty regarding whether or not to perform a release of the coracoacromial ligament during acromioplasty, as this could increase the risk of superior and anterior glenohumeral translation.<sup>9</sup></p>
<p>The <em>acromion process</em> is a triangular-like extension of the scapular spine, and anteriorly articulates with the clavicle. The acromioclavicular articulation is a synovial joint, connecting the scapula and clavicle, allowing the scapula to have multidirectional motion with relation to the rest of the body. The coracoacromial ligament forms the ligamentous attachment between the acromion and coracoid process (Figure 2). The deltoid and trapezius muscle groups have attachments on the acromion. The deltoid muscle abducts the arm at the shoulder and contraction of the trapezius rotates the scapula, providing stability to the scapular body. At birth, the distal acromion and clavicle are cartilaginous structures, but maintain the shape of the fully matured ossified bone. With maturation, the primary ossification center ossifies and proceeds to fuse with smaller secondary ossification centers to form a single fused plate. Most literature suggests these ossification centers normally ossify between 18 to 25 years of age.<sup>14</sup> Unfused secondary ossification centers may be mistaken for avulsion fractures, and primary and secondary fusion scars can mimic an incompletely healed fracture on radiographs and MRI, respectively (Figure 3). The presence of marrow edema on MR images should portend a diagnosis of fracture.<sup>15</sup></p>
<p>As stated earlier, Neer proposed that tears of the cuff tendons (specifically the supraspinatus) are often a result of impingement by structures forming the coracoacromial arch. Extrinsic impingement syndrome is clinically characterized as acute or chronic pain induced by abduction and external rotation or elevation with internal rotation of the shoulder. Impingement typically occurs in young athletes who participate in sports involving repetitive movements of elevation and abduction of the shoulder, or in the elderly population with degenerative joint disease.<sup>16</sup> Numerous anatomical etiologies have been suggested as a contributor of impingement syndrome including variant acromion shape, slope of the acromion, acromioclavicular arthropathy, acromion positioning, coracoacromial ligament thickening, and os acromiale. However, it is worth noting that many of the aforementioned anatomical factors can be seen in the asymptomatic patient, and ultimately the diagnosis is one of a clinical nature.<sup>17</sup></p>
<p>Three predominant shapes of the lateral acromion have been described by Bigliani et al and are based on the scapular-Y view radiograph.<sup>18</sup> Type I acromion has a flat undersurface (Figure 4). Type II acromion is more concave along the undersurface with the inferior acromial cortex parallel to the cortex of the humeral head (Figure 5). Type III acromion has an inferiorly projecting anterior hook, narrowing the space between the acromion and humeral head (Figure 6). Some theories suggest type II and III acromions have an increased incidence of cuff disease, but this remains controversial among most surgeons.<sup>17</sup> Type IV acromion has also recently been described as having a convex undersurface, although correlation with extrinsic impingement has not been shown.<sup>19,20</sup></p>
<p>Normal orientation of the lateral aspect of the acromion is horizontal or slightly downsloping posteriorly on the sagittal images. An abnormally sloped acromion occurs in an anteriorly downsloped and inferolateral sloped orientation (Figure 7). These anomalous acromial sloping positions can impinge on the subacromial space and cause mechanical trauma to the subjacent supraspinatus tendon.<sup>17</sup></p>
<p>Normal positioning of the acromion has an inferior cortex running parallel with the inferior cortex of the clavicle. When the acromion is low-lying, the inferior cortex of the acromion lies below the inferior cortex of the clavicle (Figure 8). This low position causes narrowing of the subacromial space.<sup>17</sup></p>
<p>Os acromiale represents an accessory ossification center that has not fused by age 25 years. This normal variant occurs in 15% of the population. Failure of fusion occurs between 1 of the 3 ossification centers: pre-acromion (Figure 9A), meso-acromion (Figure 9B), and meta-acromion. A classification scheme was proposed by Park et al with subtypes A-G. Type A, also known as the meso-acromial or meso-type, is the most common and is a failure of fusion between the meso-acromion and meta-acromion.<sup>21</sup> The presence of an os acromiale has been associated with increased incidence of impingement and rotator cuff disease, although is controversial in the literature.<sup>21,22</sup> There is suggestion that the os is mobile, and thus reduces the size of the coracoacromial arch during motion. Os acromiale can cause impingement in 2 separate manners: Contraction of the deltoid muscle will force the os acromiale inferiorly, leading to narrowing of the rotator cuff outlet. The other mechanism occurs when osteophytes develop at the margin of the acromial gap, often directly impinging on the rotator cuff.</p>
<h2>Imaging Appearance of Extrinsic Impingement</h2>
<p>The imaging findings of external impingement are varied, ranging from subacromial/subdeltoid bursitis to full-thickness rotator cuff tears. In 1972, Charles Neer classified impingement into 3 distinct stages. Stage I impingement is characterized by edema and/or hemorrhage in the subacromial/subdeltoid bursa and is generally seen in patients less than 25 years-old. Stage II demonstrates chronic changes such as fibrosis and tendinitis of the rotator cuff and is generally seen in those 25 to 40 years. Stage III is characterized by partial or complete rotator cuff tears, and is usually seen in patients &gt; 40 years.<sup>4,23</sup></p>
<p>Subacromial/subdeltoid bursitis is a finding seen with considerable frequency on MRI examinations of the shoulder (Figure 10). This diagnosis is characterized by fluid-like signal in the bursa that extends 2 cm medial to the acromioclavicular joint with distension of the bursa &gt; than 3 mm thick. Fluid also commonly extends into the anterior aspect of the bursa.<sup>24</sup></p>
<p>Rotator cuff tendinopathy (or tendinosis) is depicted by thickening and increased signal within the tendons. With tendinopathy, there is no visible discontinuity of tendon fibers and signal does not extend to the articular or bursal surface. Also, signal seen within tendinopathy is hyperintense on fluid-sensitive sequences, but is hypointense compared to nearby intra-articular fluid signal (Figure 11). Fluid-like hyperintense signal within the tendon suggests an intrasubstance partial tear.</p>
<p>Partial thickness tears of the rotator cuff are characterized by fluid-like signal in the tendons that does not involve the entire tendon bulk. These tears can be further characterized by whether they involve the bursal surface, intrasubstance portion of the tendon, or articular surface of the tendon fibers (Figures 12-14). Partial thickness tears occur more frequently along the articular surface of the tendon.<sup>25</sup> Ellman developed a classification system for partial rotator cuff tears based on the tendon tear depth. This system classifies partial thickness tears into grade I (&lt; 3 mm), grade II (3 to 6 mm), or grade III (&gt; 6 mm).<sup>26 </sup>As grade III tears comprise &gt; 50% of the rotator cuff, these are generally considered significant and are typically repaired surgically.<sup>27</sup></p>
<p>Full-thickness rotator cuff tears are manifested by fluid-like signal within the tendon, which extends throughout the entire substance of the tendon from the articular to the bursal surface (Figure 15). These can be further classified according to size. A widely used system created by DeOrio and Cofield classifies full thickness tears based on their greatest dimension. These are classified as small (&lt; 1 cm), medium (1 to 3 cm), large (3 to 5 cm), or massive (&gt; 5 cm).<sup>28</sup> Other important features of full-thickness tears are the degree of tendon retraction and presence or absence of muscle atrophy. A tendon retracted medial to the glenoid has historically indicated that the tendon tear is not amenable to repair (Figure 16).<sup>29 </sup>Muscle atrophy in association with a full-thickness tear of the supraspinatus or infraspinatus tendons suggests that the muscle has lost its ability to contract and may not be successfully treated with surgery.<sup>30</sup> This information is of clinical value to the surgeon when deciding whether to repair the tear.</p>
<p>MR characteristics of impingement have been subsequently grouped into subtypes by Seeger et al.<sup>31</sup> Type I impingement is noted as the least severe and includes subacromial bursitis and bursal thickening with normal signal intensity of the supraspinatus tendon. Type II impingement is classified as abnormally high-signal in the supraspinatus tendon without abnormal intramuscular signal or tendon retraction. Type III impingement findings include full-thickness abnormal signal intensity with muscle retraction, indicating a full-thickness tear.</p>
<p>Acromion morphology and acromion-related pathology is easily identified on MR. Acromial spurs have been described with numerous morphologic subtypes including acromial hook and keel osteophytes. The acromial hook lies within the origin of the coracoacromial ligament and projects toward the coracoid. This is located at the anterior inferior acromion.<sup>32</sup> A subacromial keel osteophyte is an acromial spur that causes severe damage to the bursal cuff and is shaped like the keel of a sailboat. The spur is found along the anterior lateral edge of the acromion, between the lateral border of the acromion and the acromioclavicular joint, and extends posteriorly to the middle of the acromion undersurface.<sup>33</sup></p>
<p>Location of the acromial spur is also important, occurring along the medial, lateral, and anterior aspects of the acromion with anterolateral spurs having a closer association with cuff pathology.<sup>34</sup> Subacromial spurs are contiguous with the cortex of the acromion undersurface with signal isointense to adjacent bone marrow on MRI (Figure 17). Acromion shape has been implicated in impingement with a classification scheme devised by Bigliani et al, as described previously. Only type III has shown a common association with impingement and rotator cuff tears, by most authors. Impingement and rotator cuff tears attributed to a type III acromion are best appreciated on the coronal and sagittal sequences.<sup>20,35</sup> The slope and angle of the acromion is also associated with extrinsic impingement. Studies have indicated that low lateral acromial angle was seen with a higher incidence of impingement. Lateral acromial angle is calculated by a vertical line lateral to the glenoid and a horizontal line parallel to the acromion surface (Figure 18). Lateral acromial angle can be seen effectively on the coronal MR image with an angle &lt; 70 degrees associated with cuff pathology.<sup>20,36</sup></p>
<p>Evaluating an os acromiale and its contribution to impingement can be challenging. On coronal and sagittal planar imaging, an os acromiale may be mistaken for a normal acromioclavicular joint. Axial imaging, usually the most cephalad image, is ideal for identifying an os acromiale. High-signal intensity on T2-weighted images may be appreciated at the synchondrosis, which may represent degenerative changes and/or instability of the os acromiale (Figure 19).<sup>21,37</sup></p>
<p>Acromioclavicular joint osteoarthritis may result in inferior projecting osteophytes or fibrosis around the joint capsule, potentially causing impingement. Inferior spurring of the distal clavicle and acromion can also cause impingement, with an inferior acromial spur associated more often with clinical symptoms. MRI appearance varies and acromioclavicular arthrosis may demonstrate marrow edema (which will have high signal intensity on T2-weighted sequences), subchondral cysts, sclerosis, and/or erosions.<sup>38</sup></p>
<p>Coracoacromial ligament (CAL) pathology has been extensively studied with regard to impingement syndrome.<sup>39</sup> The CAL is susceptible to pathological degeneration, which can thicken the ligament, greater than its normal thickness of 2 to 5.6 mm. This thickening, and associated subacromial osteophytes at the ligamentous attachment, can cause impingement on the supraspinatus tendon (Figures 20, 21).<sup>40</sup></p>
<h2>Treatment</h2>
<p>Of the nonoperative treatment options, studies have shown that exercise therapy combined with other noninvasive treatments have higher efficacy with regard to pain score.<sup>41</sup> Exercise therapy and localized drug injections showed better positive effects on pain score than any other nonoperative treatment options.<sup>41,42</sup></p>
<p>Operative treatment options for extrinsic shoulder impingement are usually related to the underlying etiological cause, and are usually reserved for cases of failed conservative treatments. One of the more common surgical procedures is subacromial decompression, which involves a subacromial bursectomy, release or retraction of the coracoacromial ligament, and removal of the subacromial spurs (Figure 22). This can be performed either as open surgery or arthroscopically. Some studies have shown that an arthroscopic approach has a better efficacy, while others show no significant difference in long-term outcome. However, it is generally accepted that arthroscopy has less of an economic burden and should be the preferred method.<sup>43,44</sup></p>
<p>CAL release is a controversial topic and resection can lead to biomechanical alteration with regard to humeral head movement. Therefore, partial release has been advocated with good long-term outcomes.<sup>39,45</sup> Limited studies have evaluated bursectomy alone vs. standard subacromial decompression, with no significant difference in clinical results between the procedures.<sup>46</sup> Acromioclavicular joint arthritis alone can be a source of pain, but has also been implicated as a cause of impingement. Distal clavicular resection, or the Mumford procedure, has been shown to improve symptomatic impingement with related acromioclavicular arthropathy as an adjunct to subacromial decompression.<sup>47,48</sup> Os acromiale treatment includes conservative measures, although patients with persistent symptomatic or functional deficits can benefit from surgical options. One of the more common procedures is an osseous fusion of the os acromiale combined with internal fixation and tension banding. This is usually followed by acromioplasty of the new acromio-acromion joint, ie, a 2-stage fusion.<sup>49</sup></p>
<h2>Conclusion</h2>
<p>Extrinsic shoulder impingement is a common cause of shoulder pain and frequently seen in clinical practice. Imaging plays an important role in identifying the cause of impingement and also in guiding clinicians with treatment planning. Understanding the anatomy, underlying mechanics, and MRI characteristics of rotator cuff impingement will allow for prompt recognition and ultimately improve outcomes.</p>
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</ol>9695MRI of the Wrist2018-07-09T15:14:52-04:002018-07-09T15:14:52-04:00Donald von Borstel, D.O., Saya Horiuchi, M.D., Nicholas Strle, D.O., Hiroshi Yoshioka, M.D., Ph.D.<p>Wrist pain is a common clinical presentation and the specific diagnosis is often challenging to obtain with clinical evaluation and radiography alone. If the patient&rsquo;s initial radiographs are noncontributory to the diagnosis, further imaging is often necessary. MRI utilization has progressively increased due to a variety of factors, including more athletic pursuits in children that may cause wrist injury, widespread availability of MRI, and improved diagnostic capabilities of wrist MRI. Therefore, MRI is a key diagnostic modality that can heavily influence treatment decisions, making it essential that radiologists effectively diagnose common wrist disorders. This review article focuses on MRI assessment of the wrist, including ligamentous injuries, carpal fractures, and various tendon pathologies, as well as patterns of advanced collapse and avascular necrosis affecting the wrist.</p>
<h2>Ligamentous Injury</h2>
<p>Imaging wrist ligaments is often challenging because they are thin and have an oblique course. The wrist ligaments are commonly divided into intrinsic and extrinsic ligaments. The intrinsic ligaments attach solely to the carpal bones, whereas the extrinsic ligaments connect the ulna, radius, or metacarpals to the carpal bones.<sup>1</sup> They are both important for maintaining carpal stability, with intrinsic ligaments being the primary stabilizers.<sup>2</sup></p>
<h3>Intrinsic Ligaments</h3>
<p>The scapholunate ligament (SLL) and lunotriquetral ligament (LTL) are essential for stability of the proximal carpal row.<sup>3</sup> For accurate injury assessment, one must be familiar with their normal variation in morphology and signal intensity.<sup>1</sup></p>
<p><em>Scapholunate Ligament Injury&mdash;</em>The SLL is horseshoe shaped with 3 components: the volar, dorsal and proximal zones. The dorsal component is approximately 3 mm thick and is associated with the joint capsule. The dorsal component is the most critical in preserving the relationship between the proximal poles of the scaphoid and the lunate.<sup>4</sup> The volar component is ligamentous and thinner than the dorsal component. The proximal component is the weakest and most susceptible to degenerative perforation.</p>
<p>MRI or MR arthrography (MRA) is of great importance in assessing the SLL. On axial images, the dorsal component is a thick, band-like structure with low signal intensity, whereas the volar component is heterogeneous (Figure 1). The proximal zone is best seen on coronal images. Although the proximal component of the SLL has a relatively similar triangular shape, it has a wide variety in shape (Figure 2). Isolated asymptomatic proximal defects are common in adults.<sup>2</sup> Tears of the SLL are diagnosed on MRI with findings of irregular morphology, abnormal signal intensity, and fluid transecting the ligaments.<sup>1</sup> A meta-analysis of the major diagnostic accuracy studies reported that the overall sensitivity and specificity of 3T-MRI for SLL tears were 75.5% and 97.1%, respectively. The sensitivity and specificity of MRA were reported as 82.1% and 92.8%, respectively.<sup>5</sup></p>
<p>Scapholunate dissociation does not occur with disruption of the dorsal component of the SLL alone. Rather, the SLL injury in combination with injury to portions of the dorsal and volar extrinsic ligaments results in the dorsiflexed intercalated segment instability (DISI) deformity with flexion of the scaphoid and extension of the lunate and triquetrum.<sup>6</sup></p>
<p><em>Lunotriquetral Ligament Injury&mdash;</em>The LTL appears V-shaped and like the SLL, consists of the volar, dorsal and proximal zones. The dorsal component is the most important in carpal stability and resistance to rotation.<sup>4</sup></p>
<p>The volar and dorsal zones appear band-like on axial images traversing between the lunate and triquetrum (Figure 1). The proximal zone is best seen on coronal images with a triangular appearance (Figure 2). Half of adults older than age 50 have communicating defects in the proximal zone of the LTL.<sup>2</sup> A few recent studies with small numbers of patients have compared the accuracy of MRI/MRA with arthroscopy. Sensitivity and specificity of MRI in detecting a complete LTL tear were 0% to 82% and 93% to 100%,<sup>7</sup> respectively; whereas sensitivity and specificity of MRA were 100% and 94% to 100%, respectively.<sup>8</sup></p>
<p>LTL injuries are a common cause of ulnar-sided wrist pain and occur with a fall onto an extended, pronated, and radial deviated hand.<sup>9</sup> Degenerative LTL tears will result from chronic ulnar impaction syndrome.<sup>10</sup> Ulnar impaction syndrome is a progressive degenerative wrist condition that occurs secondary to excessive load across the ulnocarpal joint, resulting in a degenerative triangular fibrocartilage complex (TFCC) tear, disruption of the LTL, and chondromalacia of the ulna, lunate and triquetrum. Therefore, in the setting of degenerative TFCC tears, LTL lesions require careful assessment.<sup>9</sup></p>
<h3>Extrinsic Ligaments</h3>
<p>Extrinsic ligament injuries can cause carpal instability and chronic wrist pain, especially when combined with intrinsic ligament injuries. An MR study of wrist trauma showed that 75% of patients had extrinsic ligament injuries, 60% had intrinsic ligament injuries, and almost half had combined ligamentous injuries.<sup>11</sup> Early ligament studies focused on only volar extrinsic ligaments; however, there is mounting evidence that both volar and dorsal capsular ligaments contribute to carpal function and alignment.<sup>2</sup></p>
<p><em>Volar Extrinsic Ligaments&mdash;</em>There are 3 major volar extrinsic ligaments: the radioscaphocapitate (RSC), radiolunotriquetral (RLT), and short radiolunate (SRL) ligaments (Fig- ure 3). The RSC arises from the radial styloid process volar surface, supports the scaphoid waist, and inserts to the capitate. The RSC supports scaphoid stability acting as a &ldquo;seat belt&rdquo; at the scaphoid waist.<sup>2</sup> The RLT arises from the radial styloid process volar rim, passes volar to the proximal scaphoid pole, attaches to the volar surface of the lunate, and inserts onto the triquetrum.<sup>2</sup> The RLT is clinically important for load transference and preventing ulnar translation of the carpus.<sup>2</sup> The SRL arises from the volar-ulnar aspect of the radius and attaches to the volar aspect of the lunate. Therefore, both RLT and SRL strongly anchor the lunate to the radius.</p>
<p>The normal RSC and RLT can be identified as linear hypointense structures with striated bands of intermediate signal intensity (Figure 3), whereas the SRL appears as a homogeneously hypointense focal thickening of the volar joint capsule. In the setting of trauma, the most frequently injured extrinsic ligaments were the RLT and RSC, almost half of which were associated with scaphoid injury.<sup>11</sup></p>
<p><em>Dorsal Extrinsic Ligaments&mdash;</em>Two major dorsal ligaments provide radioscaphoid stability&mdash;the dorsal radiotriquetral (DRT) and dorsal scaphotriquetral (DST) ligaments (Figure 4). These ligaments form a V-shape with the apex to the triquetrum, and can be identified as linear hypointense structures, often with striated bands of intermediate signal intensity (Figure 4).<sup>2</sup> The DRT was shown to be the third most frequently injured extrinsic ligament, and is commonly involved in triquetrum avulsions.<sup>11</sup></p>
<h2>Triangular Fibrocartilage Complex (TFCC)</h2>
<p>The TFCC is a fibrocartilage-ligament complex providing stability to the distal radioulnar joint and helps transmit axial load from the carpus to the ulna. The TFCC is an essential pivot point for forearm rotation and is highly prone to injuries.<sup>12</sup> The TFCC is comprised of an articular disc (TFC disc proper) and surrounding fibrous structures&mdash;the triangular ligament, the volar and dorsal radioulnar ligaments, the ulnolunate ligament, the ulnotriquetral ligament, the ulnar collateral ligament, and the meniscus homologue (Figure 5).<sup>13</sup> The triangular ligament has V-shaped collagen fiber bundles, which anchor the fibrocartilaginous disc proper to the tip and fovea/base of the ulnar styloid process. The volar and dorsal radioulnar ligaments form the volar and dorsal margins of the TFCC. The volar radioulnar ligament is reinforced by ulnolunate and ulnotriquetral ligaments inserting to the volar lunate and triquetrum, respectively. Although the structural terminology is still controversial, the extensor carpi ulnaris (ECU) tendon subsheath can be included as a stabilizer of the ulnar side of the TFCC. The ECU tendon changes in position between supination and pronation.<sup>14</sup></p>
<p>On coronal images, the normal disc proper shows asymmetric bowtie-like low signal intensity, whereas the triangular ligament shows a striated pattern of increased internal signal (Figure 5).<sup>15</sup> On axial images, the volar and dorsal radioulnar ligaments are well recognized as hypointense band-like structures (Figure 6). The ulnolunate and ulnotriquetral ligaments show homogeneous low-signal intensity (Figure 7).</p>
<p>Noncontrast MRI studies have shown that the overall sensitivity and specificity for TFCC injuries were 83% and 82%, respectively.<sup>16</sup> MRA was superior to noncontrast MRI in an investigation of TFCC injuries, with an overall sensitivity of 84% and specificity of 95%.<sup>17</sup></p>
<h3>MR Technique for Evaluation of the TFCC</h3>
<p>Appropriate MRI techniques should be applied for visualization of precise TFCC anatomy. Table 1 shows a detailed overview of the typical routine sequence protocols for 3T-imaging of the wrist.<sup>14</sup> Images have commonly been acquired with conventional 2-dimensional (2D) techniques; however, 3D-imaging techniques reduce partial volume artifact and can be reformatted into any cross-sectional plane from a single acquisition. Although the isotropic 3D fast spin echo (FSE) sequences suffer from relatively long acquisition time and image blurring, several advanced techniques&mdash;such as parallel imaging, short TR sequences combined with driven equilibrium, and compressed sensing&mdash;have shortened overall scan time.<sup>18</sup></p>
<h3>Traumatic TFCC Tears</h3>
<p>The Palmer classification divides TFCC tears into traumatic and degenerative lesions (Table 2).<sup>19</sup> This classification system is frequently used by hand surgeons to guide management.<sup>13</sup></p>
<p>Traumatic tears occur far less frequently than degenerative tears. The most common mechanism of traumatic TFCC injury is a fall on an outstretched hand. TFCC tears usually present clinically as ulnar-sided wrist pain and/or distal radioulnar joint instability.</p>
<p>Class I/traumatic TFCC tears are subclassified according to injury location. Conservative treatments are generally recommended; when conservative management is unsuccessful, several surgical options can be considered. The surgical treatments can be based on the TFCC lesion location. Class IA tear is at the central/paracentral region of the disc proper, which is the most common traumatic subtype of TFCC tears (Figure 8). Since the avascular central articular disc has limited healing capacity, debridement is usually performed for pain relief.<sup>20</sup> Class 1B tear is the avulsion of the triangular ligament with or without an ulnar styloid fracture (Figure 9). The instability of the distal radioulnar joint is most remarkable in Class IB injuries. Class IC tear is avulsion of the ulnolunate or ulnotriquetral ligaments, which can result in ulnocarpal instability. For Class IB and IC injuries, surgical repair may be indicated.<sup>20</sup> A Class ID tear involves either an avulsion tear of the TFCC (Figure 8) or an avulsion fracture at the sigmoid notch of the radius. When the avulsion fracture exists, a direct repair leads to better outcomes.<sup>20</sup> For a Class ID tear without avulsion fracture, various surgical repairs have been reported and ulnar shortening osteotomy may relieve the axial load on the TFCC.</p>
<p><em>Degenerative TFCC Tears&mdash;</em>Degenerative Class II TFCC lesions are subclassified with subtypes based on the progressive destruction of the TFCC and adjacent ligaments and cartilage. Class IIA lesions represent wear of the horizontal portion of the disc proper without perforation. Class IIB lesions resemble IIA lesions with additional chondromalacia of the lunate and/or ulna. Progression of the degenerative change results in perforation of the disc proper, which then is classified as Class IIC lesions. Class IID lesions represent a further advanced degenerative process with rupture of the LTL (Figure 10). Class IIE lesions describe the final stages of ulnar impaction syndrome. These findings are often associated with ulnocarpal and distal radioulnar degenerative arthritis. In the chronic phase of TFCC injury, conservative treatments are initially selected and, if unsuccessful, ulnar shortening osteotomy or ulnar head resection can be considered.<sup>20</sup></p>
<p>A cadaveric study reported that TFCC degeneration begins in the third decade, and subsequent perforations increase with age.<sup>21</sup> Similarly, MRI findings of degenerative TFCC lesions were seen with higher frequency in patients older than 50.<sup>22</sup> Traumatic and degenerative abnormalities are difficult to distinguish between and can coexist as age increases.</p>
<h2>Carpal Fractures</h2>
<p>Carpal fractures account for 21% of upper extremity fractures, with the proximal carpal row most frequently affected.<sup>23</sup> While plain film radiographs remain the initial imaging modality of choice, early MRI has proven a valuable tool for radiographically occult fractures. MRI has sensitivity and specificity rates of 80% and 100%, respectively, in radiographically occult scaphoid fractures.<sup>24</sup></p>
<p>Carpal fractures exhibit a linear hypointensity on T1-weighted imaging (T1WI) with surrounding edema (T1-hypointensity and T2-hyperintensity). Short protocol MRI exams, consisting of short tau inversion recovery (STIR) and T1WI, have shown reliable negative predictive values in the acute setting often negating unnecessary immobilization and follow-up radiation.<sup>25</sup></p>
<h3>Scaphoid Fracture</h3>
<p>The scaphoid is the most commonly fractured carpal bone, encompassing approximately 70% of all carpal fractures (Figure 11). The scaphoid is divided into proximal, middle, and distal poles, which are important to delineate when predicting long-term healing potential. There is a single intraosseous artery (branch of the radial artery) to the scaphoid, which enters the scaphoid dorsally at the midpole (waist) and supplies the proximal pole in a retrograde fashion. While the majority of fractures heal with proper treatment, approximately 15% to 30% of scaphoid fractures will develop osteonecrosis, which increases in prevalence with proximal pole and displaced fractures.<sup>26</sup></p>
<p>Up to 40% of scaphoid fractures are missed at initial presentation, and follow-up MRI of the wrist is becoming more common. A scaphoid fracture segment with hypointense T1- and T2-signal is concerning for decreased vascularity. While these findings alone are a poor predictor of impending osteonecrosis/nonunion, they should raise suspicion for potential setbacks in healing (Figure 12).<sup>27</sup> As osteonecrosis develops, the scaphoid will exhibit fragmentation and collapse.</p>
<p>Treatment of scaphoid fractures is typically achieved conservatively with immobilization. Stable, nondisplaced fractures involving the mid/distal poles achieve a union rate of 90% with casting alone.<sup>27</sup> Surgery is commonly reserved for unstable or displaced fractures, proximal pole fractures, or when nonunion/osteonecrosis occurs.</p>
<h3>Triquetral Fracture</h3>
<p>The triquetrum is the second-most commonly fractured carpal bone, accounting for 18.3% of carpal fractures.<sup>28</sup> They typically involve the dorsal cortex and are most frequently diagnosed on lateral radiographs of the wrist. Triquetral fractures are radiographically occult in up to 20% of cases.<sup>28,29</sup> On MRI, the most sensitive finding is bone marrow edema, which may even obscure the fracture line. Most commonly, the small fracture fragment is visualized within the dorsal soft tissues and follows the osseous signal on all sequences; however, diffuse soft-tissue edema may obscure these fragments.</p>
<p>It has been suggested that the dorsal fracture fragment results from a dorsal extrinsic ligament avulsion injury.<sup>28</sup> There is often combined ligamentous injury in these patients, which reinforces MRI&rsquo;s role in acute wrist injuries. Less frequent triquetral fractures involve the body of the triquetrum (typically in the setting of perilunate fracture dislocation) and volar avulsion fractures (ulnotriquetral or lunotriquetral ligament avulsion).</p>
<h3>Hamate Fracture</h3>
<p>Hamate fractures account for 1.7% of carpal fractures, with the hook of the hamate the most frequent site.<sup>29</sup> They are associated with racket sports as the handle directly compresses the protruding hook. Given the tendinous and ligamentous insertions on the hook of the hamate, associated displacement of the fragment may delay healing or nonunion. Occasionally, fractures may involve the body of the hamate, typically due to an axial loading injury or associated perilunate dislocations.<sup>26</sup></p>
<p>MRI demonstrates a T1-hypointense and T2-hyperintense fracture line (Figure 13). Comment should be made on the degree of displacement and signal characteristics of the displaced fragment, as there is increased risk of nonunion when the hook of the hamate is involved.</p>
<h2>Tendon Pathology</h2>
<h3>Normal Tendon Appearance</h3>
<p>Tendons normally have homogeneous hypointense signal on all MRI sequences. Wrist tendons are divided into the flexor and extensor subgroups, and are best appreciated in the axial plane (Figure 14)<em>.</em><sup>30</sup> Most flexor tendons traverse the carpal tunnel, with 3 located outside the tunnel: the flexor carpi ulnaris, flexor carpi radialis, and the palmaris longus (PL) tendons. The PL is not present in a minority of the population. The extensor tendons are divided into 6 compartments, each with a separate tenosynovial sheath.<sup>31</sup></p>
<h3>General Tendon Abnormalities</h3>
<p>Pathology of the wrist tendons include tendinopathy, tenosynovitis, and partial and complete tears. MRI allows the radiologist to reliably distinguish between these entities.</p>
<p><em>Tendinopathy </em>is a generalized term describing diffuse or focal tendon thickening. This is usually secondary to chronic overuse and presents with T2-hyperintense signal within the tendon substance (Figure 15A).</p>
<p><em>Tenosynovitis </em>presents with a hyperintense fluid-signal within the tendon sheath (Figures 15B, 16). The diameter of the tendon sheath fluid is greater than the tendon diameter. Fluid-like signal that does not surround the tendon is most commonly a normal finding. Usually patients with tenosynovitis or tendinopathy complain of localized tenderness, decreased grip strength, and pain with range of motion. These entities are usually related to repetitive trauma and inflammatory or infectious arthritis. Any wrist tendon may be affected; however, tendons at a point of restriction are most commonly involved (eg, the ECU tendon as it passes over the ulnar groove). They are often successfully treated with conservative therapy.</p>
<p>MRI findings of a torn tendon include a focal disruption or distorted appearance of the tendon. <em>Partial tears </em>have a focal region of hyperintense T1- and T2-signal with some fibers remaining intact (Figure 17). <em>Complete tears</em> show full-thickness discontinuity at any point of the tendon and often present with retraction of the torn tendon. Peritendinous edema and/or hemorrhage suggest an acute tear. Tendon tears are often treated conservatively with splinting. However, if conservative treatment fails or the tear is &gt; 40% thickness of the tendon, primary surgical repair is often performed.<sup>30</sup></p>
<h3>de Quervain Tenosynovitis</h3>
<p>First described in 1895, this condition is a stenosing tenosynovitis affecting the extensor pollicis brevis (EPB) and abductor pollicis longus (APL) tendons of the wrist.<sup>30,32,33</sup> This results from chronic overuse and can commonly be seen in women (particularly new mothers), racquet sports, golf, and also recently recognized in frequent texters.</p>
<p>Patients present with pain along the radial aspect of the wrist exacerbated by thumb adduction and ulnar deviation of the wrist. There can be localized swelling and tenderness. The Finkelstein test is positive when pain occurs upon passive ulnar deviation while the thumb is adducted.</p>
<p>MRI displays EPB and APL tenosynovitis with fluid-like signal within the tendon sheath. Associated tendinopathy varies from localized tendon thickening to an interstitial tear. Peritendinous edema-like signal also often surrounds the first extensor compartment (Figure 18).</p>
<p>Treatment begins conservatively with nonsteroidal anti-inflammatory drugs (NSAIDS) and immobilization with a thumb spica brace. Corticosteroid injection into the first dorsal compartment can also yield good results. Surgical decompression is reserved for patients who fail these measures.</p>
<h3>Extensor Carpi Ulnaris Injuries</h3>
<p>The ECU has unique anatomical characteristics and courses along the dorsomedial aspect of the forearm through its own fibro-osseous tunnel, in a groove between the ulnar head and the styloid process.<sup>10,14,34</sup> This tunnel is formed by the distal ulna and a band of connective tissue known as the ECU subsheath, which stabilizes the ECU as it courses over the distal ulna (Figure 19). The combination of the subsheath and extensor retinaculum prevent subluxation and friction of the ECU tendon.</p>
<h3>Extensor Carpi Ulnaris Tenosynovitis and Tendinosis</h3>
<p>These entities occur from repetitive stress causing synovial inflammation and are commonly seen in athletes, particularly rowers and racquet sport players. Typical presentation includes point tenderness and swelling at the dorsal/ulnar aspect of the wrist.</p>
<p>Progression usually begins with tenosynovitis and circumferential hyperintense T2-signal on MRI. Continued stress leads to tendinopathy and ultimately tendon tear.<sup>9</sup> A pitfall on MRI is the &ldquo;pseudolesion,&rdquo; which is when the tendon has centrally increased T1- and T2-signal on axial images at the level of the distal radioulnar joint (DRUJ). This is secondary to intrasubstance mucoid degeneration or magic angle effect.<sup>1,35</sup> Nonfocal increased signal and tendon thickening distinguish true tendinosis from a pseudolesion.</p>
<p>Nonsurgical conservative treatment is often successful with splinting of the wrist for 6 to 8 weeks. If this fails, surgical release of the sixth compartment can be performed with tendon debridement and subsheath reconstruction.</p>
<p><em>Extensor Carpi Ulnaris Subsheath Injury</em></p>
<p>The ulnar wall of the subsheath can rupture in the setting of trauma or with recurrent stress injuries. This often results in ECU subluxation, with ulnar displacement of the tendon, even if the overlying extensor retinaculum is intact.<sup>9,30</sup> The tendon commonly returns to a normal position in pronation. On MRI, the ECU is subluxed with complete tears of the ECU subsheath dorsal attachment. The volar attachment of the ECU subsheath is often lax and there is usually peritendinous edema (Figure 20).</p>
<h3>Intersection Syndrome</h3>
<p>There are 2 intersection syndromes involving the extensor tendons second compartment.<sup>31,36</sup> The <em>distal intersection syndrome</em> involves the extensor pollicis longus (EPL) as it crosses over the extensor carpi radialis longus (ECRL) and extensor carpi radialis brevis (ECRB) tendons, and is rare (Figure 21). The more common <em>proximal intersection syndrome </em>involves the APL and EPB myotendinous junctions as they cross over the ECRL and ECRB. This occurs approximately 4 to 8 cm proximal to the Lister tubercle and is known as the &ldquo;oarsmen&rsquo;s wrist,&rdquo; commonly affecting rowers and weightlifters as a result of repetitive wrist flexion/extension. MRI shows tenosynovitis involving the tendon with surrounding soft-tissue, edema-like signal.<sup>36</sup></p>
<p>These intersection syndromes are commonly treated conservatively with steroid or local anesthetic injection into the second compartment. If this fails, tenosynovectomy and decompression can be performed at the level of intersection.</p>
<h3>Scapholunate Advanced Collapse (SLAC) and Scaphoid Nonunion Advanced Collapse (SNAC)</h3>
<p>These entities represent the most common types of wrist arthritis seen by hand surgeons.<sup>37</sup> Given their prevalence and associated disability, it is important to recognize them radiographically. MRI is unnecessary for staging the disease, but displays cartilage to a much better extent.<sup>38</sup></p>
<p>SLAC wrist pattern of osteoarthritis occurs after injury or degenerative attenuation of the SLL. SNAC wrist develops following a scaphoid fracture that progresses to nonunion. There is a traditional 4-stage classification scheme of SLAC and SNAC wrists.<sup>39</sup> Stage I displays arthrosis at the radial styloid-distal scaphoid articulation. Stage II involves the proximal radioscaphoid joint in SLAC wrists and the scaphocapitate joint in SNAC wrists. Stage III involves degeneration of the midcarpal joint, and specifically the capitolunate joint (Figure 22). Stage IV involves pancarpal arthrosis with preservation of the radiolunate joint.</p>
<h3>Kienbock disease</h3>
<p>Kienbock disease is avascular necrosis of the lunate (lunatomalacia or lunate osteonecrosis). The most common theory for this entity is compromise of the lunate vasculature.<sup>40</sup> Risk factors associated with Kienbock disease include negative ulnar variance, high uncovering of the lunate, abnormal radial inclination, and trapezoidal shape of the lunate.<sup>41</sup> Without prompt diagnosis and treatment, disease progression will ultimately lead to joint destruction within 3 to 5 years.<sup>40</sup></p>
<p>The pattern of disease follows a progression delineated by the Lichtman classification, staging by lunate morphology and signal characteristics (Figure 23). In <em>stage I</em>, the lunate maintains its normal morphology, but develops a uniform edema-like pattern of diffuse T1-weighted hypointensity and hyperintense signal on fluid-sensitive sequences.<em> Stage II </em>denotes the early sclerotic changes of the lunate with hypointense signal on T1WI and variable signal on fluid-sensitive sequences. Stage II also marks the earliest findings on plain film radiography with increased density of the lunate. Progression to collapse is first demonstrated in <em>stage III</em> with loss of height in the coronal plane and lengthening of the lunate in the sagittal plane. <em>Stage IV</em> is characterized by lunate collapse along with radiocarpal and midcarpal degenerative change. In addition, an adjacent reactive synovitis and joint effusion may be associated.<sup>40</sup> If intravenous gadolinium is used during imaging, nonenhancing portions of the lunate are concerning for nonviable fragments, although late revascularization may occur.</p>
<h2>Conclusion</h2>
<p>MRI of the wrist is progressively increasing in utilization, but is often a daunting task for interpreting radiologists. Understanding the complex anatomy of the wrist and more common disease of the ligamentous, osseous, and tendinous structures allows the radiologist to efficiently and accurately evaluate MRI of the wrist with improved diagnostic capabilities. This ultimately leads to more efficient treatment and better patient outcomes.</p>
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</ol>9674The Role of Core-Needle Biopsy in the Evaluation of Head and Neck Lesions2018-04-24T16:00:28-04:002018-04-24T16:00:28-04:00Natosha Monfore, D.O., Maha Jarmakani, D.O., Jason M. Wagner, M.D.<p>Over the years, needle biopsy has dramatically changed the evaluation of head and neck lesions. Prior to routine use of needle biopsies, surgical biopsy was a primary technique for tissue diagnosis in the head and neck. However, with the improvement of image quality and development of different needle systems, fine-needle aspiration (FNA) and core-needle biopsy (CNB) have become the primary methods for making a tissue diagnosis in the thyroid and salivary glands, as well as in lymph nodes.<sup>1,2 </sup>While FNA of head and neck lesions is a well-established technique, CNB is increasingly recognized as a preferred diagnostic technique, particularly with lymph nodes and salivary gland lesions.<sup>3</sup> The goal of this article is to review the role of CNB in evaluating head and neck lesions.</p>
<h2>Overview of Biopsy Techniques</h2>
<p>Palpation-guided FNA of neck lesions is commonly performed in a clinic setting and is a reasonable initial diagnostic procedure. Image-guided FNA, however, has been shown to produce higher diagnostic yield.<sup>4-8</sup> US is the preferred method of imaging guidance, although CT guidance can be helpful for deeper lesions, particularly near the skull base.<sup>9,10</sup> FNA is performed using narrow-gauge needles (20 to 25 gauge) with the goal of removing sufficient cells for cytologic analysis. FNA biopsies can be performed with or without suction (capillary action). We generally begin with an FNA biopsy using a 25-gauge needle with capillary action and add suction or use a larger needle if the initial passes yield an insufficient sample. One benefit of US-guided FNA is its safety, with a very low incidence of significant complications.<sup>1,11,12</sup> The main disadvantage of FNA is the small sample acquired, which can lead to cases of an insufficient sample or nondiagnostic results.<sup>4,13</sup></p>
<p>CNBs are performed with larger gauge cutting needles (16 to 20 gauge) to harvest tissue fragments, allowing histologic assessment and identification of the architectural features of the specimen. There are many core biopsy devices, including semi-automated and fully automated side-cut needles as well as fully automated end-cut needles.<sup>2,14</sup> CNB has been shown to increase diagnostic yield compared with FNA biopsy of salivary lesions and cervical lymph nodes.<sup>3,15-18</sup> The principal disadvantage of CNB is the concern for a greater incidence of significant complications, including tumor implantation along the biopsy tract, hemorrhage, and damage to adjacent structures, although the actual risk is low.<sup>3,19 </sup></p>
<p>There are multiple differences between the FNA and CNB techniques. Preliminary cytologic assessment of fine-needle aspirates may be performed by an onsite pathologist, allowing real-time feedback to assess the adequacy of a sample. Although immediate assessment of core specimens is feasible with touch prep technique, core specimens are generally placed in solution to be examined after the procedure. Core specimens generally provide larger specimens for subsequent immunohistochemical analysis, although such analysis can be successful with FNA if sufficient sample is available for creation of a cell block.<sup>19</sup> With CNB there is the risk of sample bias, as often only 1 or 2 samples are obtained, whereas with FNA a larger portion of the lesion can be sampled by directing the needle throughout all portions of the lesion with real-time US guidance.</p>
<p>Image-guided head and neck needle biopsies are commonly performed using single needle technique. Coaxial technique using an introducer needle allows multiple needle samples with a single puncture and can be performed particularly with deeper lesions. Disadvantages of coaxial technique include larger needle size and the potential for introducing gas into the tissues surrounding a targeted lesion, which can impair US visualization.</p>
<p>The indications for, results of, and potential complications of CNB vary between different tissues of the head and neck. Highlighted below are the specific issues regarding CNB in the thyroid, salivary glands, and cervical lymph nodes.</p>
<h2>Thyroid Gland</h2>
<p>The thyroid gland is in the anterior cervical neck, just inferior to the larynx, in the visceral space. It is anterior to the trachea and esophagus, and medial to the carotid sheaths. The arterial supply to the thyroid is from the superior and inferior thyroid arteries. The superior thyroid artery is the first anterior branch of the external carotid artery and runs superficially along the anterolateral surface of the thyroid. The superior thyroid artery is the landmark for identifying the superior laryngeal nerve, which courses with the artery until approximately 1 cm from the superior thyroid pole. The inferior thyroid artery arises from the subclavian artery in the thyrocervical trunk. It ascends vertically, then curves medially to enter the tracheoesophageal groove in a plane posterior to the carotid space. Most of its branches penetrate the posterolateral aspect of the thyroid. Posteromedial to the thyroid is the tracheoesophageal groove where the paratracheal nodes, recurrent laryngeal nerve, and parathyroid glands are located. The recurrent laryngeal nerve is associated with the inferior thyroid artery at approximately the junction of the lower and middle thirds of the thyroid gland.</p>
<p>In 2015, the American Thyroid Association updated guidelines for the work-up of adult patients with thyroid nodules.<sup>20</sup> These recommendations combine nodule size, sonographic appearance, and clinical risk factors to determine the need for FNA, with FNA rarely indicated for nodules &lt; 1 cm. Nodules highly suspicious for malignancy based on sonographic appearance include those that are solid and hypoechoic, or have a solid hypoechoic component in a partially cystic nodule with one or more of the following characteristics: irregular margins, microcalcifications, greater height than width, rim calcification with small extrusive soft-tissue components, or evidence of extrathyroidal extension. Prior to FNA, patients should have a thorough diagnostic US examination, as findings on diagnostic US change management in more than half of patients.<sup>21</sup> Specifically, if suspicious lymph nodes are discovered, then FNA of at least one node is generally indicated.<sup>22</sup></p>
<p>When biopsy of a thyroid nodule is indicated, FNA is the procedure of choice.<sup>20,22</sup> FNA provides samples that are satisfactory for interpretation in 89% to 95% of cases; 55% to 74% of samples are definitively benign and 2% to 5% are definitively malignant.<sup>20</sup> The most significant disadvantage of FNA occurs when the cytology is nondiagnostic. According to the Bethesda System for Reporting Thyroid Cytopathology, nondiagnostic samples include atypia or follicular lesion of indeterminate significance in 2% to 18% of nodules, follicular neoplasm in 2% to 25%, and suspicious for malignancy in 1% to 6%.<sup>20</sup> In the setting of nondiagnostic cytology, repeat FNA with US guidance and onsite cytology review for adequacy is suggested and may yield a diagnostic result in 60% to 80% of nodules.<sup>20</sup> If the second US-guided FNA is also nondiagnostic, it has been shown that a third FNA is less likely to be diagnostic. At this point, further evaluation of the US characteristics can help determine the next step. If the lesion has suspicious imaging characteristics, then further workup with either CNB, molecular testing, or surgical excision should be considered.</p>
<p>The role of CNB of thyroid nodules remains controversial. In the setting of a nondiagnostic FNA, CNB has been reported to have a higher diagnostic rate than repeat FNA, with diagnostic rates of &gt; 95%.<sup>23-25</sup> CNB has also been shown to have highly diagnostic results in the setting of a calcified thyroid nodule where FNA adequacy may be difficult.<sup>26</sup> One study, however, suggested that CNB may be less sensitive than FNA for the diagnosis of malignancy.<sup>27</sup> Subsequent studies have found a higher sensitivity for detecting malignancy with CNB as compared with FNA, although CNB may be limited in the setting of a follicular lesion.<sup>23,28</sup> The limitation of CNB in the setting of follicular lesions is not surprising, as the histologic differentiation between follicular adenoma and low-grade follicular carcinoma requires evaluation of the entire specimen to detect capsular invasion.<sup>28</sup> One meta-analysis concluded that CNB had suboptimal sensitivity for malignancy (68%); however, this meta-analysis did not include the most recent reported studies.<sup>3</sup> CNB of the thyroid is considered safe by most recent reports with occasional hematomas and self-limited hemoptysis, but no major complications requiring intervention.<sup>23,25,26,28</sup></p>
<p>In the setting of a nondiagnostic thyroid nodule FNA, molecular testing of FNA samples is an option. Like CNB, the role of molecular testing has not been definitively established, particularly given the rapid advancement of molecular testing techniques.<sup>29</sup> For instance, one molecular testing technique has been reported to have sensitivity and specificity of &gt; 90% for both follicular lesions and atypia of undetermined significance.<sup>30,31</sup></p>
<p>Molecular testing is generally performed with FNA aspirates and, therefore, has the theoretical advantage of decreased risk of complications as compared with CNB. Additionally, it is possible (and our practice) to collect specimens for molecular testing at the time of the initial FNA, although this requires an additional 1 to 3 needle sticks per nodule. The molecular testing specimens can be retained in the laboratory for several months, allowing a decision on whether to send the specimen for molecular testing to be made after final cytopathology results. The major advantage of this approach is that the patient does not have to return for a second biopsy procedure.</p>
<p>In addition to primary thyroid malignancies, primary thyroid lymphoma is another important pathology to consider. Thyroid lymphoma comprises 1% to 5% of all thyroid malignancies and most commonly consists of either marginal zone (mucosa-associated lymphoid tissue) lymphoma, which has a good prognosis, or diffuse large B-cell lymphoma, which has a poor prognosis.<sup>32</sup> When the FNA results suggest lymphoma or when the clinical suspicion for lymphoma is high in the presence of a nondiagnostic FNA, subsequent collection of material for flow cytometry and CNB can be obtained <strong>(Figure 1)</strong>. CNB has been reported to have a 90% diagnostic rate for thyroid lymphoma.<sup>28</sup></p>
<h2>Salivary Glands</h2>
<p>The parotid gland is the largest of the salivary glands and lies in the parotid space, which is the most lateral major suprahyoid neck space. The parotid gland is bound superiorly by the external auditory canal, inferiorly by the mandible, anteriorly by the masticator space, and posteriorly by the sternocleidomastoid and posterior belly of the digastric muscles. The parotid gland is divided into superficial and deep lobes, which are anatomically delineated by the facial nerve. While the facial nerve cannot be directly visualized sonographically, its position can be inferred by the retromandibular vein, which commonly runs just deep to the facial nerve. The external carotid artery runs deep to the retromandibular vein and ascends through the gland to give rise to the posterior auricular, maxillary, and superficial temporal arteries. The accessory lobe of the parotid is positioned anteriorly along the parotid duct and lies superficial to the masseter muscle.<sup>33</sup></p>
<p>The submandibular glands are in the anterior portion of the submandibular triangle, below the floor of the mouth. The submandibular duct connects the gland to the floor of the mouth. Similar to the parotid gland, the submandibular gland is made up of superficial and deep lobes delineated by the mylohyoid muscle. Three nerves are closely associated with the submandibular glands: lingual, hypoglossal, and the marginal mandibular branch of the facial nerve. The lingual nerve begins lateral to the submandibular duct and courses anteromedially. The hypoglossal nerve is deep to the gland and runs superficial to the hyoglossus muscle but deep to the digastric muscle. The marginal mandibular branch of the facial nerve runs inferior to the submandibular gland. The submental arteries and veins provide blood supply to the gland.</p>
<p>US is the initial modality of choice for investigating a salivary gland lesion. MRI is a useful second-line imaging test, particularly for deep parotid lobe lesions that may be difficult to fully visualize with US due to limited deep sound penetration or when perineural spread of tumor is suspected. US guidance during needle biopsy allows for direct visualization of the needle within the mass, facilitating targeting of solid portions of the mass and avoidance of adjacent vascular structures.</p>
<p>Approximately 70% of parotid masses are neoplasms.<sup>34</sup> The differential diagnosis of parotid neoplasms is complex, as the World Health Organization (WHO) classifies 28 types of salivary malignancies, many of which have low-, intermediate-, and high-grade varieties.<sup>35</sup> Additionally, more than a dozen benign neoplasms may occur in the salivary glands.<sup>36</sup> The likelihood of malignancy for a salivary neoplasm is inversely proportional to the gland size, with 15% to 32% of parotid tumors, 41% to 45% of submandibular tumors, and 70% to 90% of sublingual tumors found to be malignant.<sup>36</sup></p>
<p>Needle biopsy of a salivary lesion is generally requested to determine whether a lesion requires surgical excision, as many salivary lesions are treated nonoperatively. Additionally, even if surgical excision is planned, preoperative diagnosis allows optimal patient counseling regarding prognosis and, in the setting of parotid tumors, the likelihood of facial nerve injury or sacrifice during surgery.<sup>35,37</sup> Although previously common, surgical incisional biopsy is now generally contraindicated because of the risks of infection, tumor seeding, facial nerve injury within the parotid gland, as well as sialocele and fistula formation.<sup>34</sup></p>
<p>Surgical biopsy has been replaced by FNA. While FNA is safe, quick and readily performed in the outpatient setting, it is not without limitations, specifically a fairly high rate of nondiagnostic samples and a limited sensitivity for malignancy. Nondiagnostic rates for salivary FNA have been reported to vary between 12% and 50%, with sensitivities varying between 64% and 88%, with considerable heterogeneity between studies.<sup>4,5,38</sup></p>
<p>CNB of salivary gland lesions has emerged as the preferred method to overcome the limitations of FNA. In three studies directly comparing FNA and CNB of salivary lesions, the nondiagnostic rate was 19% to 56% for FNA and 4% to 5% for CNB, while the sensitivity for malignancy was 60% to 76% for FNA and 89% to 93% for CNB.<sup>15-17 </sup>Typically, core biopsies are sufficient for formal histologic and immunohistochemical analysis, thus allowing for grading and typing of malignancies to include lymphoma. Also, CNB can help determine salivary gland involvement in systemic diseases such as Sj&ouml;gren disease and sarcoidosis.</p>
<p>The major concern regarding CNB of salivary lesions has been an increased risk of significant complications, such as facial nerve injury during parotid biopsies. While facial nerve injury remains a theoretical possibility, the recent literature regarding CNB of salivary masses reports only occasional minor complications such as hematoma, but no nerve injuries or other major complications.<sup>15,16,39,40</sup> A key step in avoiding nerve injury is thought to be use of careful technique that limits deployment of the cutting notch of the CNB entirely within the targeting lesion <strong>(Figure 2)</strong>.<sup>16</sup> Another potential complication is needle tract seeding with subsequent tumor recurrence; however, the exact incidence of this is unknown as tumor recurrence may be 10 or more years after the biopsy.<sup>12</sup> Tumor seeding has been rarely reported with both FNA and CNB; the risk of tumor seeding is likely less with needle biopsy than with surgical biopsy.<sup>12,34</sup></p>
<p>The safety and efficacy of CNB of salivary lesions has led some authors to recommend CNB as the initial biopsy technique, although others leave open the possibility of starting with FNA in institutions where FNA has been successful.<sup>19,37</sup> In our practice, we most commonly begin with FNA, but have a low threshold to add CNB for lesions with a solid component if the preliminary FNA results suggest nondiagnostic cytology.</p>
<h2>Lymph Nodes</h2>
<p>Cervical lymph nodes are composed of lymphoid tissue and are located along the lymphatic vessels in the neck. Each lymph node is encapsulated by fibrous tissue and contains a cortex and medulla. The cortex is composed of densely packed lymphocytes, while the medulla consists of medullary trabeculae, medullary cords and sinuses. Normal lymph nodes are ovoid or reniform in shape, with sharp distinct margins. Pathologic lymph nodes commonly exhibit alterations of shape, morphology and vascularity. Lymph nodes suspicious for malignancy are typically more round, with irregular or ill-defined margins, and may contain a central area of calcification or necrosis.<sup>41</sup> On US, this is demonstrated by a loss of the normal echogenic fatty hilum and internal heterogeneity. Normal lymph nodes show central hilar vascularity, whereas malignant nodes show eccentric or absent vascularity, peripheral perfusion, focal perfusion, or multifocal aberrant vascularity. Although larger nodes tend to have a greater likelihood of malignancy, lymph node size is a poor predictor of malignancy.<sup>41</sup></p>
<p>The anatomic location of cervical lymph nodes is based on 7 nodal stations, levels I-VII.<sup>42</sup> Level Ia nodes are submental and medial to the anterior bellies of the digastric muscles. Level Ib nodes are submandibular and are posterolateral to the anterior belly of the digastric muscles. Level II nodes are the upper jugular nodes and are anterior to the posterior border of the sternocleidomastoid muscle (SCM) and lateral to the submandibular gland. Both level I and level II nodes are bounded inferiorly by the inferior margin of the hyoid bone. Level III nodes are the middle jugular nodes between the inferior border of the hyoid bone and cricoid cartilage. Level IV are the inferior jugular nodes, located from the inferior border of the cricoid cartilage to the superior margin of the clavicle. Both level III and level IV are anterior to the posterior border of the SCM and lateral to the medial margin of the common and internal carotid arteries. Level V are posterior to the posterior border of the SCM, with Va being posterior to level II and III. Level Vb nodes are posterior to level IV and extend inferiorly to the superior clavicle. Level VI nodes are anterior to the visceral spaces from the inferior margin of the hyoid bone to the manubrium, medial to the common and internal carotid arteries. Level VII are the superior mediastinal nodes between the common carotid arteries, below the superior margin of the manubrium to the level of the brachiocephalic vein.</p>
<p>Metastatic carcinoma to neck lymph nodes tends to follow predictable patterns in an untreated neck. Oropharyngeal squamous cell carcinoma, which is often associated with the human papilloma virus (HPV), tends to spread to bilateral level II and level III lymph nodes.<sup>43</sup> Oral cavity cancer, including anterior tongue, lips, and floor of mouth tumors, typically involves level I or level II lymph nodes.<sup>44</sup> Cutaneous primary squamous cell carcinoma of the midface and scalp most commonly spreads to intraparotid lymph nodes, followed by level II and level V nodes.<sup>45</sup> Papillary thyroid cancers tend to metastasize to levels III, IV and VI. In papillary thyroid cancer, level II involvement is less common and level I involvement is rare, although any lymph node level may be involved with widespread disease.<sup>46</sup> Metastatic disease to neck lymph nodes from an infraclavicular primary tends to most prominently involve the supraclavicular lymph nodes (at the inferior aspect of level IV and Vb).<sup>41</sup> Lymph node involvement of lymphoma can include any nodal basin in the neck, including the intraparotid nodes.</p>
<p>US-guided needle biopsy is well established in the evaluation of neck lymph nodes, although the procedural approach should be customized for each patient based on the clinical scenario. In a patient with a suspicious cervical node, or cluster of nodes, and no history of malignancy, the most likely diagnoses are reactive/infectious adenopathy, lymphoma, and metastasis from an unknown primary malignancy. In this situation, we begin with US-guided FNA. If the preliminary cytopathology yields a polymorphous population of lymphocytes with no suspicious cells and our clinical suspicion based on the patient presentation and sonographic appearance of the nodes is low, then we stop with FNA.</p>
<p>If there is a greater suspicion for malignancy, then we will add FNA passes for flow cytometry. Flow cytometry can be performed with both FNA and core samples, as long as the samples are placed in the appropriate medium, such as the Roswell Park Memorial Institute (RPMI) solution. Whether FNA or core specimens are preferred for flow cytometry is a matter of institutional preference. With a high level of suspicion based on clinical presentation or preliminary cytopathology, then we will add a core biopsy <strong>(Figure 3)</strong>. As compared with FNA alone, CNB has been shown to increase the diagnostic yield for lymphoma and decrease the need for excision biopsy.<sup>47</sup> A recent meta-analysis found CNB to have a sensitivity of 92%, specificity of 93%, and accuracy of 92% in distinguishing lymphoma from reactive adenopathy.<sup>3</sup></p>
<p>In a patient with a recently diagnosed primary malignancy and neck lymph nodes suspicious for metastasis, we find that FNA is frequently sufficient to confirm metastasis, provided that the primary malignancy has been sufficiently sampled and there is no need for further pathologic evaluation or molecular testing. In a patient with suspected infraclavicular primary malignancy without a pathologic diagnosis and suspected neck node metastasis, the neck nodes are an excellent location to sample the disease, due to the ease of sampling the neck and the very low rate of significant complications. In this setting, CNB is frequently indicated to allow for complete pathologic and molecular tissue evaluation.<sup>48</sup></p>
<p>Suspicious cervical lymph nodes in a patient previously treated for papillary thyroid carcinoma (PTC) is a unique but commonly encountered situation. Lymph nodes containing metastatic PTC commonly have cystic changes, calcification or hyperechoic foci, and disordered vascularity<strong> (Figure 4)</strong>. Although CNB may have a role in highly selected cases of metastatic thyroid cancer, tissue thyroglobulin assay is the test of choice for suspicious lymph nodes with negative cytology in a patient with a history of PTC.<sup>49,50</sup> When we perform FNA of a suspicious lymph node in a patient with a history of PTC, we essentially always collect material (one FNA pass washed in 1cc of saline) for tissue thyroglobulin assay, unless the preliminary cytopathology is unequivocally positive.</p>
<h2>Conclusion</h2>
<p>Fine-needle aspirations and core-needle biopsies have supplanted surgical biopsies for most head and neck lesions. Although these procedures are not immune to the risk of complications, the use of image guidance has increased their safety and efficacy. CNB in particular has well-established indications for head and neck masses involving salivary glands, particularly the parotid gland, and cervical lymph nodes. Its use in the assessment of thyroid lesions remains controversial with the rapid advancement of molecular testing techniques that can be used with thyroid FNA samples. In the end, the decision to use FNA vs CNB needs to be based on the specific and sometimes unique presentation of each case.</p>
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<li>Pratap R, Qayyum A, Ahmed N, et al. Ultrasound-guided core needle biopsy of parotid gland swellings. J Laryngol Otol 2009;123(4):449-452.</li>
<li>Eom HJ, Lee JH, Ko MS, et al. Comparison of fine-needle aspiration and core needle biopsy under ultrasonographic guidance for detecting malignancy and for the tissue-specific diagnosis of salivary gland tumors. Am J Neuroradiol 2015;36(6):1188-1193.</li>
<li>Haldar S, Mandalia U, Skelton E, et al. Diagnostic investigation of parotid neoplasms: a 16-year experience of freehand fine needle aspiration cytology and ultrasound-guided core needle biopsy. Int J Oral Maxillofac Surg 2015;44(2):151-157.</li>
<li>Saha S, Woodhouse NR, Gok G, et al. Ultrasound guided core biopsy, fine needle aspiration cytology and surgical excision biopsy in the diagnosis of metastatic squamous cell carcinoma in the head and neck: an eleven year experience. Eur J Radiol 2011;80(3):792-795.</li>
<li>Haldar S, Sinnott JD, Tekeli KM, et al. Biopsy of parotid masses: review of current techniques. World J Radiol 2016;8(5):501-505.</li>
<li>Haugen BR, Alexander EK, Bible KC, et al. 2015 American Thyroid Association Management Guidelines for Adult Patients with Thyroid Nodules and Differentiated Thyroid Cancer: The American Thyroid Association Guidelines Task Force on Thyroid Nodules and Differentiated Thyroid Cancer. Thyroid 2016;26(1):1-133.</li>
<li>Marqusee E, Benson CB, Frates MC, et al. Usefulness of ultrasonography in the management of nodular thyroid disease. Ann Intern Med 2000;133(9):696-700.</li>
<li>Frates MC, Benson CB, Charboneau JW, et al. Management of thyroid nodules detected at US: Society of Radiologists in Ultrasound consensus conference statement. Ultrasound Q 2006;22(4):231-238; discussion 239-240.</li>
<li>Na DG, Kim JH, Sung JY, et al. Core-needle biopsy is more useful than repeat fine-needle aspiration in thyroid nodules read as nondiagnostic or atypia of undetermined significance by the Bethesda system for reporting thyroid cytopathology. Thyroid 2012;22(5):468-475.</li>
<li>Yeon JS, Baek JH, Lim HK, et al. Thyroid nodules with initially nondiagnostic cytologic results: the role of core-needle biopsy. Radiology 2013;268(1):274-280.</li>
<li>Screaton NJ, Berman LH, Grant JW. US-guided core-needle biopsy of the thyroid gland. Radiology 2003;226(3):827-832.</li>
<li>Ha EJ, Baek JH, Lee JH, et al. Core needle biopsy can minimise the non-diagnostic results and need for diagnostic surgery in patients with calcified thyroid nodules. Eur Radiol 2014;24(6):1403-1409.</li>
<li>Renshaw AA, Pinnar N. Comparison of thyroid fine-needle aspiration and core needle biopsy. Am J Clin Pathol 2007;128(3):370-374.</li>
<li>Hahn SY, Shin JH, Han BK, et al. Ultrasonography-guided core needle biopsy for the thyroid nodule: does the procedure hold any benefit for the diagnosis when fine-needle aspiration cytology analysis shows inconclusive results? Br J Radiol 2013;86(1025):20130007.</li>
<li>Ferraz C, Eszlinger M, Paschke R. Current state and future perspective of molecular diagnosis of fine-needle aspiration biopsy of thyroid nodules. J Clin Endocrinol Metab 2011;96(7):2016-2026.</li>
<li>Nikiforov YE, Carty SE, Chiosea SI, et al. Highly accurate diagnosis of cancer in thyroid nodules with follicular neoplasm/suspicious for a follicular neoplasm cytology by ThyroSeq v2 next-generation sequencing assay. Cancer 2014;120(23):3627-3634.</li>
<li>Nikiforov YE, Carty SE, Chiosea SI, et al. Impact of the multi-gene thyroseq next-generation sequencing assay on cancer diagnosis in thyroid nodules with atypia of undetermined significance/follicular lesion of undetermined significance cytology. Thyroid 2015;25(11):1217-1223.</li>
<li>Nachiappan AC, Metwalli ZA, Hailey BS, et al. The thyroid: review of imaging features and biopsy techniques with radiologic-pathologic correlation. Radiographics 2014;34(2):276-293.</li>
<li>Ramachar SM, Huliyappa HA. Accessory parotid gland tumors. Ann Maxillofac Surg 2012;2(1):90-93.</li>
<li>Kuan EC, Mallen-St Clair J, St John MA. Evaluation of parotid lesions. Otolaryngol Clin N Am 2016;49(2):313-325.</li>
<li>Lewis AG, Tong T, Maghami E. Diagnosis and management of malignant salivary gland tumors of the parotid gland. Otolaryngol Clin N Am 2016;49(2): 343-380.</li>
<li>Guzzo M, Locati LD, Prott FJ, et al. Major and minor salivary gland tumors. Crit Rev Oncol Hematol 2010;74(2):134-148.</li>
<li>Howlett DC, Skelton E, Moody AB. Establishing an accurate diagnosis of a parotid lump: evaluation of the current biopsy methods - fine needle aspiration cytology, ultrasound-guided core biopsy, and intraoperative frozen section. Br J Oral Maxillofac Surg 2015;53(7):580-583.</li>
<li>Liu CC, Jethwa AR, Khariwala SS, et al. Sensitivity, specificity, and posttest probability of parotid fine-needle aspiration: a systematic review and meta-analysis. Otolaryngol Head Neck Surg 2016;154(1):9-23.</li>
<li>Schmidt RL, Hall BJ, Layfield LJ. A systematic review and meta-analysis of the diagnostic accuracy of ultrasound-guided core needle biopsy for salivary gland lesions. Am J Clin Pathol 2011;136(4):516-526.</li>
<li>Howlett DC, Menezes LJ, Lewis K, et al. Sonographically guided core biopsy of a parotid mass. Am J Roentgenol 2007;188(1):223-227.</li>
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<li>Corey A. Pitfalls in the staging of cancer of the oropharyngeal squamous cell carcinoma. Neuroimag Clin N Am 2013;23(1):47-66.</li>
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</ol>9652Common Pitfalls in Oncologic FDG PET/CT Imaging2018-01-23T12:22:51-05:002018-01-23T12:22:51-05:00Benjamin L. Viglianti, M.D., Ph.D., Ka Kit Wong, M.B.B.S., Milton D. Gross, M.D., Daniel J. Wale D.O.<p>Over the last decade, F-18 fluorodeoxyglucose (FDG) PET/CT has continued to have an ever-increasing role in staging malignancy, evaluating tumor response to treatment, and evaluating indeterminate masses discovered on CT, MRI and US. Many decisions regarding medical and/or surgical interventions are largely based on functional metabolic information gathered from the PET/CT. It is, therefore, critical for the interpreting physician to be aware of potential pitfalls that may lead to an erroneous diagnosis.</p>
<p>As the name implies, FDG is an analog of glucose that is beneficial in detecting a variety of malignancies. The relative increased uptake of FDG by many malignancies compared to background tissues is due to the increased expression of glucose transporters by cancer cells, as well as variations of intracellular enzyme activity with increased activity of hexokinase and decreased activity of glucose-6-phosphatase.<sup>1</sup> Ultimately, this leads to increased accumulation of FDG in many malignant cells as, unlike regular glucose, FDG does not become further metabolized after initial phosphorylation.</p>
<p>Unfortunately for interpreting physicians, a major limitation of FDG is that it is not specific for neoplastic cells. In addition to the variations of normal human metabolism within organs and tissues that universally rely on glucose as a substrate, a variety of nonmalignant inflammatory processes can also demonstrate significant FDG uptake. In fact, FDG is increasingly used clinically for nononcological purposes, including neurodegenerative disorders, cardiac viability, cardiac sarcoid, as well as replacing traditional radiolabeled leukocyte imaging for detecting infection. There is also an overlap in the amount of FDG uptake between many benign and malignant lesions. This problem is common in evaluating solitary pulmonary nodules and incidental adrenal nodules, for example. Furthermore, certain benign lesions such as Warthin&rsquo;s tumors may also display a high degree of FDG uptake.</p>
<p>Additionally, whole-body FDG PET/CT is a technically challenging examination compared to many standard radiology studies. Patient preparation, radiotracer injection, uptake period, image acquisition, and processing all have potential for problems that can affect image interpretation.</p>
<p>This article is a pictorial review of a variety of pitfalls in interpreting FDG PET/CT scans. After discussing a variety of general considerations, details of pitfalls related to specific body regions will be presented. With familiarity and understanding of these processes, the reading physician increases the likelihood of diagnostic pitfall recognition, thus avoiding incorrect interpretations.</p>
<h2>General Considerations</h2>
<p>Although patient preparation can vary by institution, practice guidelines from the Society of Nuclear Medicine and Molecular Imaging suggest that patients fast 4 to 6 hours prior to PET imaging to ensure optimal insulin levels.<sup>2</sup> Injection of FDG and subsequent imaging in nonfasting patients can result in a so-called <em>altered biodistribution</em>, in which there is relative increased FDG uptake throughout the body&rsquo;s skeletal muscles largely due to insulin effect (<strong>Figure 1</strong>). Similar findings can be seen in patients on insulin and corticosteroids, as well as in those who have recently exercised. Regardless of cause, an altered biodistribution can obscure underlying disease and potentially affect tumor-to-background conspicuity.<sup>3 </sup></p>
<p>Similarly, artifacts can be related to suboptimal injection technique of the radiopharmaceutical. A small amount of extravasation at the injection site is common, and correlation with injection site documentation is advised when identifying a small focus of abnormal uptake in the subcutaneous tissues of the upper extremities or in draining lymph nodes. However, occasionally a greater amount of the radiotracer extravasates, causing more significant artifacts (<strong>Figure 2</strong>). The interpreting physician must use caution when reporting such cases and may need to repeat the study to ensure diagnostic accuracy. Specifically, the calculated standardized uptake values (SUVs) of the lesions of concern may not be accurate as the documented injected dose (one parameter for determining SUV) likely does not reflect the true dosage of FDG in the blood pool due to the extravasation.</p>
<p>In addition to the usual motion artifacts present throughout imaging modalities, PET/CT is susceptible to potentially problematic artifacts when patient position changes between CT and PET acquisition, resulting in misregistration. This is common near the diaphragm, as most PET acquisition is not done with a breath-hold, although respiratory gating can help minimize this misregistration. With more significant motion, FDG uptake can project over the incorrect anatomic structures and may lead to incorrect localization (<strong>Figure 3</strong>). Some software packages allow the user to adjust registration to align data to correct the error, although these are usually limited to rigid realignments in 3 axes. Patient motion between the PET and CT portion of the studies can also cause an incorrect attenuation map to be applied to the PET region, thus affecting the attenuated corrected data set.</p>
<p>In addition, metal or other high-density implants, as well as oral and intravenous contrast, can create a false area of relative increased uptake due to attenuation correction artifacts. Attenuation correction works well in the range of tissue densities within the human body; however, it is prone to falsely overestimate the degree of attenuation correction in regions of higher density materials. As this activity is usually not associated with anatomic masses, it is usually discounted by the interpreter by noting the CT findings. However, review of the nonattenuation corrected data set can confirm the artifact, as this activity should disappear on nonattenuation-corrected images.<sup>4</sup></p>
<p>Lymphoma is one of the more common indications for oncological PET/CT. Some of the most common histological subtypes, including Hodgkin disease and diffuse large B-cell lymphoma, are extremely PET-avid, and PET can be used for staging and assessing treatment response. However, other histological subtypes are less likely to be FDG-avid. These include primary cutaneous anaplastic large T-cell lymphoma, extranodal marginal zone lymphoma, and small lymphocytic lymphoma.<sup>5</sup> When performing initial staging PET/CT on patients with a known lymphoma, occasionally a non-FDG avid lymphoma will be encountered. It is important to alert the referring physician that the disease being evaluated is not FDG-avid and a follow-up FDG PET/CT for determining treatment response may not be useful. Knowledge of neoplasms that have low FDG avidity is important to prevent inappropriate action regarding false-negative findings, including hepatocellular carcinoma, renal cell carcinoma, neuroendocrine tumors, well-differentiated endocrine malignancy, prostate cancers and some genitourinary cancers.</p>
<h2>Pediatric Variants, Pitfalls and Artifacts</h2>
<p>PET imaging for childhood cancers is predominately performed for lymphoma, osteosarcoma, Ewing sarcoma, and soft-tissue sarcomas including rhabdomyosarcoma and malignant peripheral nerve sheath tumors. Imaging children requires specific knowledge of changes in the physiological processes of maturation; the more frequent need for sedation; and awareness of the spectrum of childhood cancers, genetic predisposition syndromes, and secondary cancers after treatment.<sup>6</sup></p>
<h3>Brown Fat</h3>
<p>Brown fat contains metabolically active mitochondria that burn energy and release heat. Brown fat uptake has been reported in one-third of children imaged with PET, and is more frequent in children than adults. It is more common in cold climates and can be reduced by warming techniques.<sup>6</sup> Common locations include the supraclavicular fossa, cervical and axillary soft tissues, mediastinum, thoracic parascapular and paraspinal soft tissues, and the upper abdomen (<strong>Figure 4</strong>).<sup>7</sup></p>
<h3>Marrow</h3>
<p>Red marrow is more metabolically active than yellow marrow and, therefore, demonstrates relatively increased FDG uptake. In neonates, the distribution of red marrow involves the distal long extremities. As infants grow, the red marrow shifts from the skull and extremities to the axial skeleton (spine, pelvic bones, ribs and sternum) with yellow fatty marrow replacement occurring earlier at the epiphyses and diaphysis (<strong>Figure 5</strong>). By around 15 years of age, this process is largely complete. In adults, only a little hemopoietic red marrow remains in the proximal metaphysis of the femur and humerus. Additionally, the skeleton in children is rapidly growing at the physes and synchondroses, which can appear relatively &ldquo;hot&rdquo; on PET imaging.<sup>8</sup></p>
<h3>Thymus</h3>
<p>Children, adolescents, and young adults have a greater incidence of thymus visualization on PET imaging, with hyperplasia occurring in the setting of severe stress or chronic disease, termed <em>thymic rebound</em> when found after chemotherapy. With maturity, the thymus varies considerably in shape, and often can be difficult to distinguish from an anterior mediastinal mass. Neonates have a large thymus, which increases up to 2 years of age. It can cover both the left and right aspects of the heart, and has been described as quadrangular. Gradually, the thymus assumes the more classic <em>sail</em> or <em>spinnaker </em>sign. On PET imaging, the thymus should have uniform FDG uptake and smooth convex margins. Cervical thymic extension is an important variant to recognize, wherein thymic tissue extends into the superior mediastinum and lower neck (<strong>Figure 6</strong>). This represents an embryologic remnant along the track of descent. It may occasionally appear as a lower cervical mass, discontinuous with the thymus, and can be mistaken for a tumor or enlarged lymph node.<sup>9</sup></p>
<h3>Lymphoid Tissue</h3>
<p>Children have prominent lymphoid tissue compared to adults, including the above-described thymus and in bone marrow. They also have prominent secondary lymphoid tissue, including the adenoid, palatine, and lingual tonsils. Furthermore, they are more prone to symmetric low-grade FDG uptake in reactive lymph nodes due to inflammation or infection in common sites, including cervical, axillary, mesenteric, and inguinal lymph nodes.</p>
<h2>Head and Neck</h2>
<p>Evaluation for brain masses is potentially problematic, largely due to the high physiologic FDG uptake in the gray matter structures. It is critical for the interpreting physician to adjust the window to detect potential hypermetabolic brain masses, such as those resulting from lymphoma, metastatic melanoma, or lung cancer (<strong>Figure 7</strong>). On the other hand, brain lesions with significant cystic and/or necrotic components may appear relatively photopenic (<strong>Figure 8</strong>). When encountering subtle foci, it is best to correlate with contrast-enhanced, diagnostic quality CT or MR. Other causes of photopenic defects in the brain include postoperative changes and prior infarcts (<strong>Figure 9</strong>).</p>
<p>In patients with no history of head and neck cancer, incidental asymmetric uptake in the pharynx poses a diagnostic dilemma, as both malignancy and infection/inflammation can result in focal asymmetric uptake (<strong>Figure 10</strong>).<sup>10</sup> Focal uptake at the midline of the nasopharynx has also been described in inflamed Thornwaldt&rsquo;s cysts. Despite a variety of attempts to find a reliable prospective means to differentiate benign from malignant uptake,<sup>11-13</sup> there is no clinical consensus for a reliable absolute or relative SUV to differentiate inflammation from malignancy. Ultimately, clinical and/or endoscopic evaluation will likely be needed to exclude malignancy.<sup>14</sup></p>
<p>Recent phonation will increase FDG uptake in the vocal cords. When this is symmetric, no diagnostic challenge is present. Focal asymmetric uptake in the vocal cords, however, likely requires further investigation. A common cause of asymmetric uptake is unilateral vocal cord paralysis. Vocal cord paralysis will result in decreased FDG uptake in the affected cord and a search for an underlying cause, such as a thoracic mass impinging the recurrent laryngeal nerve, cervical mass involving the course of the vagus nerve, or history of neck surgery (<strong>Figure 11</strong>). In the absence of an underlying cause, laryngoscopy will likely be necessary.</p>
<p>As with pediatric patients, brown fat FDG uptake is a common cause of focal uptake in adult necks, and is potentially problematic when evaluating patients with head and neck cancers as well as lymphoma.<sup>15</sup> The key for identifying this pitfall is localization of the uptake to fat density on CT and lack of corresponding soft-tissue mass. At times, however, it can be difficult to separate this activity from closely adjacent lymph nodes. This entity occurs more in colder climates. Because brown fat is sympathetically innervated, patient anxiety at the time of the PET scan may contribute to its visualization. A variety of means can help minimize this brown fat uptake, the simplest of which is to ensure adequate warming prior to injection and uptake.<sup>16</sup> Several drugs, including propranolol,<sup>17</sup> diazepam,<sup>18</sup> and fentanyl,<sup>19</sup> have also shown to decrease brown fat uptake; however, the routine clinical implementation of these medications is challenging in the outpatient setting. Although uncommon, hibernomas, which are benign neoplasms composed of brown fat, can demonstrate increased FDG uptake.</p>
<p>Incidental uptake in the thyroid gland is often encountered on PET imaging. Diffuse increased FDG uptake throughout the thyroid gland is usually benign; correlation can be made for diffuse thyroid diseases, including Graves&rsquo; disease or chronic lymphocytic (Hashimoto&rsquo;s) thyroiditis (<strong>Figure 12</strong>).<sup>20</sup> Although rare, diffuse FDG uptake has been associated with malignancy, including cases of thyroid lymphoma<sup>21</sup> and metastatic non-small cell lung carcinoma.<sup>22</sup> Focal thyroid FDG uptake, on the other hand, requires additional evaluation with ultrasound and possible tissue sampling, as there is a significant association with malignancy. In one study, Choi et al demonstrated malignancy in 18 of 49 focal thyroid lesions detected on FDG PET/CT and it is generally accepted that one-third of FDG-avid thyroid nodules are malignant, with the remainder being benign thyroid adenomas (<strong>Figure 13</strong>).<sup>23</sup></p>
<p>Muscle uptake in the neck is variable and mostly related to recent use, pain, anxiety or inflammation. As with brown fat uptake, this muscular uptake can be readily localized to muscle with CT correlation and the lack of a correlating mass lesion. Regardless, this should be minimized, particularly when evaluating patients with head and neck cancer, as this uptake may obscure small disease foci. Most patient protocols request withholding eating and chewing gum prior to the exam, as this can result in intense FDG uptake throughout the muscle of mastication (<strong>Figure 14</strong>).</p>
<p>Additional hypermetabolic lesions may be encountered incidentally in the head and neck. Most commonly, these include incidental foci in the salivary glands (<strong>Figure 15</strong>) and sinuses (<strong>Figure 16</strong>). When encountering such lesions, it is appropriate to suggest additional work-up with imaging and/or tissue sampling. Seo et al documented focal FDG uptake in the parotid gland in 2.1% of patients with head and neck malignancy, of which 33.3% were metastatic foci disease and 66.7% demonstrated a variety of benign pathologies.<sup>24</sup></p>
<h3>Thorax</h3>
<p>Evaluation of the solitary pulmonary nodule is one the most common indications for FDG PET/CT, which aids characterizaion of indeterminate pulmonary nodules. In a study evaluating 89 patients with solitary pulmonary nodules, FDG PET/CT demonstrated a sensitivity of 92% and speficity of 90% for detecting malignancy.<sup>25</sup> However, smaller nodules pose potential problems given the spatial resolution of PET (7 to 8 mm).<sup>26</sup> Both the 2013 American College of Chest Physicians practice guidelines for pulmonary nodules and the 2017 Fleischner Society guideines for incidental pulmonary nodules have indications for FDG PET/CT for nodules &gt; 8 mm.<sup>27,28 </sup>In routine clinical practice, any non-FDG avid nodule <u>&lt;</u> 8 mm should be considered too small to accuretely characterize by PET, and continued CT followup should be considered to ensure stability.</p>
<p>In addition to issues with small pulmonary nodules, PET/CT has been shown to be less sensitive for several types of pulmonary malignancy. Adenocarcinoma in situ (formerly called bronchoalveolar carcinoma) and carcinoid are classically associated with being falsely PET negative,<sup> </sup>although other low-grade or early broncogenic malignancies have also been shown to be falsely PET negative.<sup>29</sup> Given the relatively low metabolic rate of these malignancies, it is necessary to continue CT surveilance of pulmonary nodules that demonstrate low (less than mediastinal vascular blood pool) FDG uptake (<strong>Figure 17</strong>). Continued follow-up is recommended, as the referring physician may not be aware of these potentially significant false negatives. The 2017 Fleischner Society guidelines provide generally accepted follow-up intervals for indeterminate pulmonary nodules. If a non-FDG avid nodule demonstrates enlargement at follow-up, tissue sampling should be considered.</p>
<p>A variety of infectious or inflammatory processes can be incidentally detected on PET/CT. Unfortunately, there is no reliable SUV threshold that can routinely differentiate infection/inflammation from malignancny with certain infectious/inflammatory processes being hypermetabolic and certain malignancies being non-FDG avid, including cystic or necrotic neoplasms.<sup>30 </sup>Additionally, measured SUVs depend on numerous factors independent of the target lesion of concern, including body fat composition, uptake time, and patient blood glucose levels.<sup>31</sup> In the chest, pneumonia, tuberculosis, mycobacteria avium complex, aspergiollosis, sarcoidosis, rheumatoid nodules, postsurgical inflammatory changes, talc pleurodesis, esophagitis, and postradiation inflammation are common (<strong>Figures 18-20</strong>). The sequelae of chronic granulomatous infections often include FDG-avid lung nodules and mediastinal lymph nodes that are often calcified.</p>
<p>Cardiac uptake is highly variable in fasting FDG PET/CT, ranging from essentially background to diffuse, intense FDG uptake. This is largely due to the heart&rsquo;s ability to metabolize carbohydrates or fatty acids with a switch to glucose in the presence of insulin or glucose loading.<sup>32</sup> Unfortunately, this makes interpreting PET findings challenging. Occasionally, an infarct may be encountered as a focal area of photopenia (<strong>Figure 21</strong>). Although uncommon, malignancies can occasionally involve the heart with regions of hypermetabolic activity, most often due to metastases with primary cardiac neoplasms being rare (<strong>Figure 22</strong>).<sup>33</sup></p>
<h2>Abdomen and Pelvis</h2>
<p>The adrenal glands are common locations for metastases and, therefore, should be closely evaluated on oncological PET/CT. Studies have shown PET/CT to be reasonably sensitive and specific for differentiating benign from malignant lesions.<sup>34</sup> However, one must be careful not to misdiagnose a variety of common benign adrenal processes as metastases (eg, adrenal adenomas, hyperplasia, myelolipomas, benign pheochromocytomas, oncocytomas, hemorrhage, and cysts), as some of these benign entities can demonstrate mild FDG uptake (<strong>Figure 23</strong>).<sup>35</sup> Although no absolute SUV threshold exists for differentiating benign from malignant uptake, Boland et al suggest a combination of CT characteristics (&lt; 10 HU indicating a benign adenoma) and ratio of adrenal lesion to liver background PET activity (with a ratio of &gt; 1 suspicious for malignancy) to be a reasonable means to characterize adrenal lesions as malignant with a sensitivity of 100% and specificity of 99%.<sup>36</sup></p>
<p>Expected uptake in the uterus and ovaries depends on a patient&rsquo;s menopausal status. Uptake in the endometrium can vary during the menstrual cycle, with greatest levels during menstrual flow and ovulatory phases.<sup>37</sup> This can pose particular diagnostic problems when evaluating women with cervical carcinoma. Consideration may be given to coordinating PET/CT with menstrual cycle phase to perform the PET/CT in the late secretory or early proliferative phases (just before or after menstruation).<sup>38</sup> Increased FDG uptake can also be seen in uterine fibroids; however, PET cannot reliably distinguish leiomyomas from leiomyosarcomas (<strong>Figure 24</strong>).<sup>39,40 </sup>Similarly, ovarian activity in premenopausal women can be physiologic and related to ovulation (<strong>Figure 25</strong>).<sup>37 </sup>In postmenopausal women, focal increased FDG uptake in either the endometrium or the ovary should be further evaluated to exclude malignancy.</p>
<p>Other portions of the genitourinary system may pose difficulty for the interpreting physician, largely due to the high physiologic FDG uptake in the urine, which can obscure small disease foci. It is advisable to adjust PET window and fusion level to avoid missing subtle lesions (<strong>Figure 26</strong>). Similarly, due the relatively high background uptake in the kidneys, FDG PET/CT has questionable utility in characterizing renal masses (<strong>Figure 27</strong>),<sup>41</sup> although higher-grade, clear-cell and papillary subtypes have been shown to have greater activity than renal background.<sup>42</sup> Additionally, pooling of radioactive urine in the ureters can often be difficult to distinguish from retroperitoneal or pelvic lymph nodes, often at the pelvic brim where the ureters cross the psoas muscles.</p>
<p>FDG uptake in the bowel continues to present a diagnostic challenge, as the uptake is highly variable. When focal FDG uptake is identified, further investigation (usually with endoscopy) is recommended, as there is an association with malignant and premalignant conditions.<sup>43</sup> Additionally, correlation with CT findings is warranted, as this may reveal an underlying infectious or inflammatory process such as appendicitis, diverticulitis, or inflammatory bowel disease (<strong>Figure 28</strong>).<sup>44</sup> Metformin, an oral diabetic medication, results in diffuse intense uptake in the colon as well as the small bowel (<strong>Figure 29</strong>).<sup>45</sup> This can unfortunately obscure metabolic activity from foci of malignancy, warranting consideration of holding the medication prior to FDG PET/CT imaging. Postsurgical changes from certain urinary diversion procedures also can result in intense bowel activity as FDG-avid urine enters the bowel (<strong>Figure 30</strong>).</p>
<h2>Muskuloskeletal</h2>
<p>Focal FDG uptake can be identified in both pathological and nonpathological fractures (<strong>Figure 31</strong>). Some studies indicate that relatively high SUVs suggest malignant pathological fractures,<sup>46,47 </sup>although no absolute SUV can be used in routine clinical practice to reliably differentiate benign from malignant fractures.<sup>48</sup> Correlation with the co-acquired CT for features suggesting a benign or malignant process is suggested. If the focus of uptake remains indeterminate, consideration can be given to MR if it would change clinical management. Alternatively, attention should be given on follow-up PET/CT, as the activity from benign post-traumatic or postsurgical fractures should normalize over several months.<sup>49</sup></p>
<p>Diffuse red marrow uptake on FDG PET/CT is another common pattern of normal variant uptake. This is most often related to bone marrow stimulation with drugs such as filgrastim and pegfilgrastim. Given the marrow stimulation, this may also result in increased uptake in the spleen.<sup>50</sup> Given the history of marrow stimulation, the interpreting physician can readily identify this marrow uptake as benign. However, occasionally the diffuse uptake can obscure previously present hypermetabolic osseous foci, making it difficult to evaluate response to treatment (<strong>Figure 32</strong>). Waiting several weeks after discontinuation of such drugs will help decrease this uptake, but must be balanced with the need for timely clinical results.</p>
<p>Patients who have undergone prior radiation therapy may have relative decreased marrow uptake in affected areas (<strong>Figure 33</strong>).<sup>51</sup> Knowledge of treatment history and location is beneficial in PET interpretation to identify this unusual pattern of uptake. The interpreting physician must be mindful to not misinterpret the normal, nonirradiated marrow as pathologic.<sup>52</sup></p>
<h2>Conclusion</h2>
<p>Oncologic FDG PET/CT is prone to many pitfalls and incidental findings, largely related to whole-body imaging and the nonspecific mechanism of FDG. This article reviewed a variety of processes that can lead to potential false-positive and false-negative findings. Interpreting radiologists must maintain constant vigilance for these common pitfalls.</p>
<h2>References</h2>
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</ol>9650Parathyroid Adenoma Evaluation Utilizing SPECT/CT Imaging2018-01-23T11:53:24-05:002018-01-23T11:53:24-05:00Daniel J. Wale, D.O., Benjamin L. Viglianti, M.D., Ph.D., Ka Kit Wong, M.B.B.S., Milton D. Gross, M.D.<p>Primary hyperparathyroidism is a common endocrine disorder classically manifesting with elevated serum parathyroid hormone and calcium levels. The most common cause of primary hyperparathyroidism is a parathyroid adenoma, and the treatment of choice is surgical removal. Modern surgical management benefits from presurgical evaluation and localization of suspected abnormal gland(s), with a shift toward minimally invasive approaches. Complementing anatomic imaging, nuclear medicine offers unique functional evaluation of parathyroid glands that can be used in the workup of patients with hyperparathyroidism.</p>
<p>Historically, it was common to rely solely on planar imaging for identifying parathyroid adenomas in hyperparathyroidism. However, planar imaging is limited by the lack of precise anatomic localization and overlapping of radioactivity from other background tissues. This is particularly problematic in parathyroid scintigraphy, as it is often necessary to distinguish overlying thyroid from closely adjacent parathyroid activity. Combining anatomic information and localization of functional imaging using contemporary SPECT/CT affords more precise localization necessary to guide presurgical treatment planning. In this article, we review imaging protocols, scintigraphic findings, and pitfalls in parathyroid scintigraphy with an emphasis on SPECT/CT imaging.</p>
<h2>Primary Hyperparathyroidism</h2>
<p>Most people have 4 parathyroid glands in the neck located posterior to the thyroid gland, where any of the 4 glands may be the site(s) of adenoma formation. There are instances, however, of more or fewer than 4 glands with supernumerary parathyroid glands being more common, occurring in about 10% to 13% of cases.<sup>1,2</sup> Furthermore, parathyroid glands may be ectopic, occurring in 16% of cases in one series of 231 patients.<sup>3</sup> Inferior glands (62%) were more often ectopic, which is likely related to the relatively longer path of migration of the inferior glands during embryologic development. Although highly variable, common locations of ectopic glands include the thymus, superior mediastinum, intrathyroidal, tracheoesophageal groove, and retroesophageal regions. Depending on location of the ectopic gland(s), the surgical access may change from a cervical to a transthoracic approach.</p>
<p>A solitary parathyroid adenoma is the most common cause of primary hyperparathyroidism, occurring in approximately 80% of cases. The remaining cases are usually due to multigland hyperplasia, multiple parathyroid adenomas or, rarely, parathyroid carcinoma (&lt; 1%).<sup>4</sup> Certain inherited diseases include a predisposition for parathyroid adenomas/hyperplasia, most notably multiple endocrine neoplasia (MEN) Types 1 and 2A.</p>
<p>Patients with hyperparathyroidism may present with a variety of nonspecific signs and symptoms including vague musculoskeletal pain, abdominal pain/renal calculi, and cognitive changes and/or depression. More commonly, patients today are often asymptomatic with abnormal parathyroid hormone and calcium levels detected on routine serum screening.<sup>5</sup> Surgery is considered the definitive treatment and is generally recommended in patients with symptoms referable to hyperparathyroidism. In otherwise asymptomatic patients, surgery or medical follow-up is recommended. In 2013, the International Workshop on the Management of Asymptomatic Primary Hyperparathyroidism proposed consensus guidelines for surgical intervention in patients without symptoms.<sup>6</sup> Surgery should be considered in asymptomatic patients who wish for definitive treatment and do not desire longer-term medical surveillance. Surgery is also recommended in asymptomatic patients ages 49 years or younger, or who have any of the following: osteoporosis or evidence of vertebral fractures on imaging, renal calculi, decreased creatinine clearance (&lt; 60 cc/min), hypercalcuria (&gt; 400 mg/24 hours), or hypercalcemia &gt; 1.0 mg/dL above normal.</p>
<p>Surgical procedures vary per healthcare facility and local surgical preference. It is critical for the interpreting imager to be familiar with the possible procedure(s) that the referring surgeon performs and how imaging findings (or lack thereof) affect procedure choice. Exploration of the bilateral neck allows the surgeon to identify normal glands and to remove enlarged or otherwise abnormal parathyroid glands. In this so-called &ldquo;bilateral 4-gland&rdquo; technique, preoperative scintigraphy can exclude an ectopic adenoma and lead the surgeon to the suspected location of the abnormal gland if one is identified on imaging. More limited approaches, whereby the surgeon may opt for a unilateral procedure choosing the side most likely to contain the adenoma based on imaging, have the advantage of reduced surgical and recovery time, fewer scars, and similar rates of successful cure compared to bilateral approaches. If the initial site of exploration is unremarkable, or if intraoperative parathyroid hormone levels fail to confirm the expected decline in levels after resection of a suspected adenoma, the surgical approach can be modified to a bilateral neck exploration. Whether unilateral or bilateral, an open or minimally invasive (endoscopic, video-assisted, robotic, etc.) procedure may be planned based on imaging findings.</p>
<p>Additionally, other intraoperative assistance may affect the procedure. Much like nuclear lymphoscintigraphy, a hand-held gamma probe may be used intraoperatively to guide identification of the parathyroid adenoma. This technique requires the surgery to be performed on the same day as nuclear imaging, or an additional injection of tracer must be administered on the day of the planned surgery. The surgeon may also monitor intraoperative serum parathyroid hormone level sampling shortly (about 10 minutes) after the removal of a suspected adenoma with an expected significant decrease (&gt; 50% decline from preoperative levels) with successful removal of the offending gland. If a significant decrease is not identified, the surgeon can opt for additional parathyroid gland exploration to locate other hyperfunctioning glands.<sup>7</sup></p>
<h2>Radiopharmaceuticals and Imaging Protocols</h2>
<h3>Overview</h3>
<p>Parathyroid nuclear imaging has evolved as radiotracers and imaging techniques become available. Historically, TI-201 was often used. TI-201 demonstrates uptake in both the thyroid and parathyroid glands, and was often performed in conjunction with a radioiodine or pertechnetate thyroid scan. So-called &ldquo;subtraction scintigraphy&rdquo; removed counts originating from the thyroid from that of the TI-201 scan to &ldquo;reveal&rdquo; a parathyroid adenoma. TI-201 ultimately fell out of favor for parathyroid imaging when a newer perfusion-based radiotracer, Tc-99m sestamibi, became available. Tc-99m sestamibi proved an effective radiotracer in localizing parathyroid adenomas compared to TI-201.<sup>8</sup> Additional advantages of Tc-99m sestamibi include less radiation exposure and a more optimal photopeak for gamma camera imaging. The greater retention of Tc-99m sestamibi in parathyroid adenomas vs. normal thyroid tissues allows for temporal separation of thyroid from parathyroid tissues based on early versus delayed postinjection imaging.</p>
<p>Contemporary parathyroid scintigraphy is based on Tc-99m sestamibi. Imaging protocols vary among institutions, and practice guidelines regarding parathyroid scintigraphy are available from national societies such as the Society of Nuclear Medicine and Molecular Imaging.<sup>9 </sup>Most parathyroid scintigraphy protocols call for either dual-time-point imaging with a single radiotracer (Tc-99m sestamibi) or dual radiotracer imaging combining thyroid with parathyroid scintigraphy.</p>
<h2>Single Radiopharmaceutical Dual-time-point Technique</h2>
<p>The simplest, most common protocol is dual-time-point imaging with two sets of images, early and delayed, after a single injection of Tc-99m sestamibi. Tc-99m sestamibi is a perfusion agent used in a variety of nuclear medicine studies including parathyroid imaging, myocardial perfusion imaging, and breast imaging. It is lipophilic and is thought to localize to the intracellular mitochondria. As with other Tc-99m-labeled radiopharmaceuticals, it has a photopeak of 140 keV and a half-life of 6 hours. The typical dose is 20 to 30 mCi, and is administered intravenously.<sup>9</sup> Imaging is performed early, at 10 to 20 minutes, and delayed at 2 to 2.5 hours (<strong>Figure 1</strong>). Longer delayed imaging times have not been found to improve the distinction of parathyroid adenomas from thyroid tissue.</p>
<p>Tc-99m tetrofosmin is a similar perfusion radiopharmaceutical also commonly used in myocardial perfusion imaging that has potential applicability in parathyroid imaging. However, in a study comparing sestamibi to tetrofosmin, tetrofosmin demonstrated less intense uptake in parathyroid adenomas compared to background thyroid uptake.<sup>10</sup> This makes tetrofosmin a less ideal radiopharmaceutical compared to sestamibi for dual-time-point imaging.</p>
<h2>Dual Radiotracer Technique</h2>
<p>Instead of dual-time-point imaging with sestamibi, thyroid imaging (with Tc-99m pertechnetate or I-123 sodium iodide) can be combined with parathyroid imaging (with Tc-99m sestamibi or tetrofosmin). As Tc-99m pertechnetate and I-123 localize to the thyroid without significant parathyroid activity, the images can be compared and digitally subtracted to detect a parathyroid adenoma.</p>
<p>However, dual-tracer techniques can be technically challenging, making implementation difficult. Theoretically, parathyroid and thyroid imaging could be obtained on two separate days allowing for decay of the initially used tracer. However, multiple day studies are not practical for most patients. Therefore, a variety of single-day protocols exist.<sup>9,11 </sup>Regardless of protocol, both images need to be normalized to allow subtraction to occur. After normalization, the I-123/Tc-99m pertechnetate image can be subtracted from the Tc-99m sestamibi/tetrofosmin image. The result would be an image of only parathyroid glands, allowing identification of the abnormal gland(s). Images could also be critiqued for thyroid nodules that may complicate interpretation. To minimize artifacts on the subtraction imaging, patient positioning must be near identical for both scans. Additionally, movement should be minimal, as excessive motion artifacts will also lead to artifacts on subtraction imaging.</p>
<p>To minimize these artifacts, Hindi&eacute; et al have proposed an imaging protocol in which the thyroid and parathyroid scans are obtained simultaneously, which requires the use of I-123.<sup>12</sup> Tc-99m pertechnetate cannot be used since it has the same photopeak as Tc-99m sestamibi and tetrofosmin at 140 keV. As I-123 has a different photopeak (159 keV) than Tc-99m-sestamibi and tetrofosmin, image acquisition may be performed simultaneously.</p>
<p>Regardless of whether I-123 or Tc-99m pertechnetate are used to image the thyroid gland, there are additional inherent limitations of dual-radiotracer imaging. A second radiotracer will increase examination costs, especially with the use of cyclotron-produced I-123. A second radiotracer also will increase radiation exposure of the patient.</p>
<h2>Future Possibilities with PET</h2>
<p>Given the increased resolution of PET and near widespread availability of PET/CT cameras, there has been a significant academic and clinical interest in developing a suitable PET radiopharmaceutical for localization of a hyperfunctioning parathyroid gland.</p>
<p>Unfortunately, the most readily available and clinically familiar PET radiopharmaceutical, F-18 fluorodeoxyglucose (FDG), is not particularly useful in detecting parathyroid adenomas.<sup>13</sup> In a small case series of 8 patients with surgically proven parathyroid adenomas or hyperplasia, Sisson et al did not find a single case of abnormal uptake on FDG.<sup>14</sup></p>
<p>Both C-11 choline and C-11 methionine have shown potential use in detecting parathyroid adenomas.<sup>13,15</sup> However, the 20-minute half-life of C-11 will likely limit clinical use to large facilities with access to onsite PET isotope production and synthetic capabilities.</p>
<p>F-18 fluorocholine is currently the most likely PET radiopharmaceutical to have widespread appeal in the clinical imaging of parathyroid adenomas. The F-18 label with 110-minute half-life allows for commercial distribution. Recent studies demonstrate F-18 fluorocholine to be sensitive in evaluating parathyroid adenomas.<sup>16,17</sup> In a study comparing F-18 fluorocholine to Tc-99m sestamibi for parathyroid imaging, both radiotracers demonstrated 100% specificity, with F-18 fluorocholine demonstrating 92% sensitivity compared to 64% from Tc-99m sestamibi.<sup>18</sup> Although further work is required, this is an intriguing radiotracer with potential clinical implications.</p>
<h2>Imaging Findings</h2>
<p>Tc-99m sestamibi accumulates in normal thyroid tissue as well as abnormal parathyroid tissue. Classically, the radiotracer washes out of the thyroid gland faster than the parathyroid adenoma. Thus, on early imaging, depending on location(s), parathyroid adenomas may be readily identified or obscured by otherwise physiologic thyroid uptake (<strong>Figure 2).</strong> On delayed imaging, thyroid activity should diminish, revealing a parathyroid adenoma (<strong>Figures 3 and 4</strong>).</p>
<h2>SPECT/CT Imaging</h2>
<p>SPECT/CT imaging with complementary anatomic and functional mapping has special applicability in parathyroid scintigraphy. Given the relative small size of parathyroid adenomas, closely adjacent viscera, and incidence of minor and major ectopy, SPECT/CT combines imaging modalities in an advantageous way to assist in localization and surgical treatment planning (<strong>Figures 5 and 6</strong>).</p>
<p>Neumann et al evaluated dual-isotope SPECT and SPECT/CT in primary hyperparathyroidism. Although sensitivities were similar, SPECT/CT was more specific, 96% compared to 48% for SPECT.<sup>19</sup> A meta-analysis of 24 studies, however, demonstrated the superior sensitivity of SPECT/CT compared to SPECT and planar techniques.<sup>20</sup> Dual-phase Tc-99m sestamibi SPECT/CT showed an estimated pooled sensitivity of 86% (CI 81% to 90%), which was superior to that of SPECT at 74% (66% to 82%) and planar imaging 70% (61% to 80%). The rate of ectopic parathyroid adenomas ranged from 4% to 20%, and most authors found that SPECT/CT was superior to SPECT and planar imaging for localization of ectopic glands (<strong>Figure 7</strong>).</p>
<p>Most clinical protocols use both planar and SPECT/CT imaging. A large field of view, parallel-equipped collimated gamma camera planar image of the neck and chest can be obtained to evaluate for glandular ectopy. High-resolution planar, pin-hole collimator imaging of neck for fine detail is also likely beneficial. This, combined with SPECT/CT of the neck and chest, yields the greatest amount of functional information (<strong>Figure 8</strong>).</p>
<h3>Imaging Pitfalls</h3>
<p>The reported performance of parathyroid scintigraphy varies in the literature. In a meta-analysis, Gotthardt et al reviewed 52 studies involving parathyroid scintigraphy in which sensitivities ranged from 39% to &gt; 90%.<sup>21</sup> Several factors likely played a role in this variable rate of false negative studies.</p>
<p>Parathyroid adenomas must be sizable for detection. In a study evaluating 107 parathyroid adenomas, the sensitivity in glands &gt; 500 mg was 91% compared to 80% in glands &lt; 500 mg.<sup>22</sup> In another study comparing characteristics of true positive and false negative parathyroid adenoma Tc-99m sestamibi images, the average true positive had a mean weight of 1336 mg, with the mean weight of false negatives of 475 mg.<sup>23 </sup>Additionally, due to their deeper location, superior parathyroid adenomas are more likely to be missed by parathyroid scintigraphy.<sup>23,24 </sup></p>
<p>Although single-gland disease is much more common, multigland disease poses substantial diagnostic challenges. One study estimated multigland disease to occur in at least 11% of cases of sporadic (nonfamilial) primary hyperparathyroidism.<sup>25</sup> Unfortunately, multigland disease is less likely to be detected by parathyroid scintigraphy. Nichols et al demonstrated a sensitivity of planar and SPECT parathyroid scintigraphy in multigland disease of 66%, compared to 90% for single-gland disease.<sup>26</sup> Differences in sensitivity persisted when taking gland size into account. In the setting of glandular hyperplasia, hyperplastic glands tend to be smaller compared to parathyroid adenomas.<sup>27</sup> Similar findings have been described with hybrid SPECT/CT imaging.<sup>28</sup> The incidence of multigland disease and its poor preoperative imaging detection have been used as arguments against unilateral gland surgery.<sup>25</sup></p>
<p>Several molecular observations also have been described to explain variations of radiopharmaceutical uptake in abnormal parathyroid glands. Parathyroid glands are primarily composed of chief and oxyphil cells. Oxyphil cells demonstrate an abundance of mitochondria, an important site of accumulation of perfusion-based imaging agents. Melloul et al demonstrated a correlation between the intensity of the radiotracer uptake with oxyphil content.<sup>29</sup></p>
<p>The expression of p-glycoprotein and/or multidrug resistance-related protein may also affect scintigraphic visualization of parathyroid adenomas. These cell membrane pumps have a negative effect upon cellular accumulation of lipophilic agents such as sestamibi.<sup>30</sup> Kao et al evaluated 47 parathyroid adenomas, 39 of which did not express p-glycoprotein or multidrug resistance-related protein and were detected on parathyroid scintigraphy.<sup>31</sup> The 8 expressing p-glycoprotein and/or multidrug resistance-related protein were not detected on scintigraphy. This expression is believed to account for the so-called &ldquo;rapid washout&rdquo; parathyroid adenomas, in which the adenoma may be seen on early images (if not obscured by the thyroid gland). However, the adenoma is no longer visualized on delayed imaging due to the efflux of the radiopharmaceutical secondary to membrane pump overexpression. Given this unusual pattern of uptake, the exam may be falsely interpreted as negative (<strong>Figure 9</strong>).</p>
<p>A variety of nonparathyroid processes can result in focal tracer uptake. This is largely related to the nonspecific nature of perfusion radiotracers. Most common and problematic is a variety of thyroid processes that can result in persistent diffuse or focal radiotracer uptake. Thyroid nodules/adenomas can demonstrate focal radiotracer uptake resulting in a false-positive study.<sup>32</sup> Certain malignant processes can demonstrate focal radiotracer uptake, of which breast, lung, and head and neck cancers would most likely be in the field of view. Brown adipose tissue uptake in the neck as a mimicker of parathyroid disease has also been described, which can be confidently evaluated with SPECT/CT.<sup>33</sup> Technical issues can also result in abnormal uptake. Most commonly extravasation in an upper extremity injection site can result in venolymphatic uptake in the upper arm with or without axillary lymph node uptake (<strong>Figure 10</strong>).</p>
<h2>Conclusion</h2>
<p>Parathyroid scintigraphy continues to play an ever-important role in preoperative evaluation in patients with hyperparathyroidism as the trend toward minimally invasive procedures continues to increase. A successful nuclear medicine specialist must have a strong fundamental understanding of the physiology and pathology of hyperparathyroidism and mechanisms of radiotracer localization. Additionally, an appreciation of imaging pitfalls, both false negative and positive, can aid image interpretation and communication with referring physicians. Hybrid SPECT/CT has additional benefits for both the radiologist and surgeon as precise localization and anatomic correlation increases reader confidence and can aid in presurgical planning. As this technology becomes more available, SPECT/CT should be routinely performed as an integral part of the contemporary approach to parathyroid scintigraphy.</p>
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<li>Hindi&eacute; E, Zanotti-Fregonara P, Tabarin A, et al. The role of radionuclide imaging in the surgical management of primary hyperparathyroidism. J Nucl Med 2015;56(5):737-744.</li>
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<li>Michaud L, Burgess A, Huchet V, et al. Is 18F-fluorocholine-positron emission tomography/computerized tomography a new imaging tool for detecting hyperfunctioning parathyroid glands in primary or secondary hyperparathyroidism? J Clin Endocrinol Metab 2014;99(12):4531-4536.</li>
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</ol>9627Utilization of Breast MRI for Extent of Disease in Newly Diagnosed Malignancy2017-10-12T14:42:10-04:002017-10-12T14:42:10-04:00Kathy M. Borovicka, M.D., Sara K. Boyd, D.O., Julia D. Cameron-Morrison, D.O., Julia J. Hobson, D.O.<p>Breast cancer remains the second leading cause of cancer-related death in women, with an approximately 1 in 8 (12%) chance of developing invasive breast cancer in a woman&rsquo;s lifetime.<sup>1</sup> Over the past two decades, significant advances in MRI have increased sensitivity in detecting breast cancer. Since then, radiologists, surgeons and oncologists have been utilizing breast MRI for both screening and staging of breast cancer. Numerous studies have shown that breast MRI can identify additional foci of carcinoma within the breasts and that it determines more extensive disease compared to conventional imaging of mammography and ultrasound.<sup>2</sup> This article will review how radiologists can use breast MRI in detecting additional disease within the breast and surrounding tissues.</p>
<h2>Limitations of Mammography and Ultrasound in Breast Cancer Detection</h2>
<p>Breast carcinomas are detected via screening and diagnostic evaluations. The workup of abnormalities includes evaluation with diagnostic mammography and ultrasound (US). Tomosynthesis is used as a 3-dimensional (3D) digital mammogram that has been shown to increase detection of invasive carcinomas.<sup>3</sup> Tissue sampling for pathologic diagnosis is then performed depending on the modality in which the abnormality is best visualized, including ultrasound guidance, stereotactic biopsy, and tissue sampling with MRI. Ultrasound-guided biopsies are preferred given the ease of performing and scheduling these cases. The radiologist must then determine whether the pathology result is concordant or discordant with the imaging findings. If discordant, a recommendation for additional tissue sampling via biopsy or surgical excision is then given.</p>
<p>While most primary lesions are found with mammography and ultrasound, these modalities have limitations. The most significant limitation with mammography is increased density of the fibroglandular tissue within the breasts, which may obscure carcinoma.<sup>4</sup> Mammography has been shown to have decreased sensitivity for detecting masses in extremely dense breasts. Additionally, these women have an increased relative risk for breast cancer compared to the average woman, with approximately a 4- to 6-fold increased risk.<sup>4,5</sup> For this reason, legislation is now in place to notify women with heterogeneous and extremely dense breasts, and 32 states require patients to be notified regarding their breast density and the possibility of additional screening, including whole-breast ultrasound and breast MRI depending on individual risk.<sup>6</sup> Decreased sensitivity of mammography is also noted in women with breast implants.<sup>7</sup> Breast ultrasound has its own limitations. It is operator dependent, with handheld scanning ultrasound most widely used. Ultrasound is also limited in evaluating or identifying calcifications.<sup>8</sup></p>
<h2>Current Role of Breast MRI</h2>
<p>Breast MRI aids with the limitations of mammography and US, and has been shown to have the highest sensitivity of the 3 modalities, helping to detect cancers that are clinically, mammographically and sonographically occult.<sup>2,9,10</sup> Indications for screening breast MRI include high-risk patients such as women with a lifetime risk &gt; 20%, women with a BRCA mutation or a first degree relative of a BRCA carrier, history of chest radiation, and women with hereditary syndromes such as Li-Fraumeni.<sup>10</sup> Breast MRI is used to determine the extent of invasive carcinomas and carcinoma in situ prior to treatment; assess response to neoadjuvant chemotherapy, metastatic carcinoma where the primary is unknown and suspected to be of breast origin; and problem solving for clinical or imaging findings. Breast MRI has also been used for assessment following surgery, as in cases with positive margins post lumpectomy; assessment for recurrence; and in cases with postoperative tissue reconstruction in which recurrence within tissue transfer flaps is suspected.<sup>10</sup></p>
<h2>BI-RADS for Breast MRI</h2>
<p>The 2013 American College of Radiology (ACR) Breast Imaging Reporting and Data System (BI-RADS) 5 lexicon provides terminology that guides radiologists in the evaluation and description of breast MRI findings.<sup>11</sup> This includes description of the amount of fibroglandular tissue and background parenchymal enhancement. Abnormalities are further characterized into a focus, mass and nonmass enhancement. A focus is focal enhancement that is &lt; 5 mm and considered to be a part of the parenchymal background enhancement. Masses are characterized by shape, margin and internal enhancement with an irregular shape and margin being most concerning. Nonmass enhancement is further characterized by distribution and internal enhancement. Linear and segmental distribution and clumped or clustered ring enhancement are most concerning.<sup>11</sup></p>
<p>The morphology of a mass is more important than the enhancement kinetics. In terms of enhancement patterns, washout kinetics are of greatest concern, although many carcinomas are of mixed kinetics, including washout, persistent and plateau. If additional suspicious masses and enhancement patterns are detected that would impact surgical and oncologic management, then a BI-RADS of 4 or 5 is given to obtain a tissue diagnosis.<sup>11</sup></p>
<h2>Breast MRI for Extent of Disease</h2>
<p>Preoperative breast MRI is increasingly used in staging newly diagnosed breast cancers. It is primarily utilized to look for evidence of more extensive disease than is noted on conventional imaging with diagnostic mammography and ultrasound. This includes additional disease in the ipsilateral or contralateral breast (<strong>Figures 1-3</strong>).</p>
<p>Location of the cancer in the breast is described in terms of breast quadrant (inner upper, inner lower, outer upper, and outer inner), depth (anterior, middle and posterior), and the o&rsquo;clock position. Size of the mass or nonmass enhancement is described in all 3 dimensions: anteroposterior, transverse and craniocaudal dimensions. These descriptors are important for localization in terms of surgery and radiation, as well as when comparing the sizes and locations to mammography and ultrasound. If additional suspicious findings are detected, multifocal disease (within the same quadrant) and multicentric disease (within at least 2 quadrants) is described.<sup>12</sup> More extensive disease also needs to be described: extension to the nipple and skin, lymphadenopathy (axillary, internal mammary and supraclavicular), involvement of the pectoralis musculature and chest wall, and osseous metastases (<strong>Figure 4</strong>).<sup>11</sup></p>
<p>On conventional imaging, the area of tissue involved is underestimated by approximately 14% on mammography and 18% on US, and only identified as more extensive with MRI (<strong>Figure 5</strong>).<sup>13</sup> In the ipsilateral breast, additional suspicious lesions have been seen in approximately 29% of individuals with confirmed malignant lesions in 16% of cases (<strong>Figure 6</strong>).<sup>2,13</sup> In the contralateral breast, MRI detects additional suspicious lesions in up to 19%, with synchronous contralateral breast malignancy found in approximately 4% of cases.<sup>2,13</sup> This contralateral disease has been found to be ductal carcinoma in situ (DCIS) in 35% of cases.<sup>14,15</sup> Biopsy is required to prove additional disease to be a malignancy since this impacts surgical management, including wider local excision or mastectomy depending on the extent of disease.<sup>13,16</sup></p>
<p>Involvement of the regional lymph nodes in breast cancer has an impact on prognosis and can affect treatment planning. MRI is useful in detecting axillary, supraclavicular and internal mammary lymph node involvement (<strong>Figure 7</strong>). Abnormal lymph nodes include loss of the normal reniform shape, loss of the normal fatty hilum, hilar compression, or diffuse or focal thickening of the cortex &gt; 3-4 mm.<sup>12</sup></p>
<p>Extension of tumor to the chest wall (<strong>Figure 8</strong>), defined as invasion of the serratus anterior, ribs or intercostal muscles, upgrades tumor stage regardless of tumor size. Invasion of the pectoralis muscle is not considered chest wall invasion and does not change the staging. Pectoralis involvement is defined as enhancement of the pectoralis muscle, which will impact surgical excision. MRI is the imaging modality of choice in assessing pectoralis muscle and chest wall involvement. Distant metastasis is seen in approximately 4% of breast cancer cases. Osseous, liver and lung metastasis may be seen with the breast MRI.<sup>17</sup></p>
<h2>Conclusion</h2>
<p>Breast MRI has been shown to be significantly more sensitive in evaluating the extent of disease in breast cancer patients when compared to mammography and US. This includes involvement of the unilateral and contralateral breast, as well as extramammary spread of disease. With a preoperative breast MRI, it is important for the radiologist to appropriately describe the extent of suspected disease in accordance with the BI-RADS lexicon, and make appropriate management and follow-up recommendations.</p>
<h2>References</h2>
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